HIV-Viral Hepatitis - A Guide For Primary Care

a guide for primary care
HI V/ Viral hepatitis
ashm
Australasian Society for HIV Medicine Inc
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The Australasian Society for HIV Medicine is the peak representative professional body for medical
practitioners and other health care workers in Australasia who work in HIV and related disease areas.
It was formed in 1988 (as the Australian Society of AIDS Physicians). It changed its name in 1989 to
reect a broader membership base and was incorporated in New South Wales in 1990.
The Society is a key partner in the Australian response to HIV, hepatitis and related diseases. It
works closely with government, advisory bodies, community agencies and other professional
organisations. It conducts a broad Education Program in HIV and viral hepatitis for medical
practitioners, health care providers and allied health workers and manages programs of continuing
medical education in HIV and viral hepatitis.
ASHM is governed by an elected voluntary board and managed by a small secretariat. It receives
support from the Commonwealth Department of Health and Ageing, State and Territory Departments of
Health and the pharmaceutical industry. ASHM convenes standing committees on a range of issues
affecting its members including education, HIV treatment, viral hepatitis, international/development
issues and professional affairs.
Benets of ASHM membership:
Journal Club, a bi-monthly publication reviewing relevant international journal articles, is mailed to
members and is available on the website: www.ashm.org.au
ASHMNews, the members newsletter, is mailed to members every second month and is also
available on the website.
The ASHM Directory of HIV, hepatitis and related services is designed as a desktop compendium of
useful contacts. It is released in print form in June/July each year. The Directory is on the website
and updated regularly.
The ASHM annual conference provides a timely forum for information exchange from the medical,
scientic and community sectors.
ASHM members receive a discount on conference registration, educational resources and
registration in the continuing medical education activities. Some educational resources are free.
Members involved in education or teaching activities can access resources from the Society.
ASHM holds report-back sessions from major conferences around the world for members and
makes these available through the website and/or on CD or printed format.
Members can also enjoy a reduced subscription to HIV Medicine, ASHMs refereed journal,
published by the British HIV Association and the European AIDS Clinical Society.
By maintaining a comprehensive database of its members interests, ASHM can alert its members
to specic issues and promote various activities to them.
About ASHM
Australasian Society for HIV Medicine, LMB 5057 Darlinghurst NSW 1300 Australia
Ph: 61-2-8204 0700 Fax: 61-2-9212 2382 Email: ashm@ashm.org.au Website: www.ashm.org.au
Editors
Gregory Dore BSc, MBBS, FRACP, MPH
Andrew Grulich MBBS, FAFPHM, MSc, PhD
Jennifer Hoy MBBS, FRACP, Grad. Dip. Epidemiology and Biostatistics
Michael Kidd MBBS, MD, DCCH, Dip. RACOG, FRACGP
Ronald McCoy MBBS, FRACGP
Anne Mijch MBBS, FRACP, Grad. Dip
Simone Strasser MBBS, MD, FRACP
HI V/ Viral hepatitis
ashm
Australasian Society for HIV Medicine Inc
HIV/Viral hepatitis: a guide for primary care
is published by the
Australasian Society for HIV Medicine (ASHM)
Locked Bag 5057, Darlinghurst, NSW 1300
Telephone (61) (02) 8204 0700
Facsimile (61) (02) 9212 2382
Email ashm@ashm.org.au
Website http://www.ashm.org.au
First published 2001
Reprint (with some revisions) 2004
Editors: Gregory Dore, Andrew Grulich, Michael Kidd, Jennifer Hoy, Ronald McCoy,
Anne Mijch, Simone Strasser
Executive Editor: Megan Nicholson
Production Editor/Project Coordinator: Vanessa Sparrow
Education Program Manager: Julie Letts (to July 2001), Edward Reis (from August 2001)
Evaluation: Lou McCallum
Printed by: Finsbury Printing, Adelaide
HIV/Viral hepatitis: a guide for primary care.
Bibliography.
Includes index.
ISBN 1 920773 12 6
1. Hepatitis - Patients - Care. 2. Hepatitis - Nursing. 3. HIV-positive persons - Care.
4. HIV infections - Nursing. I. Dore, Gregory John, 1962- .
II. Australasian Society for HIV Medicine.
616.3623
Australasian Society for HIV Medicine Inc. 2004
ABN 48 264 545 457
CFN 17788
Apart from any fair dealing for the purpose of research or study, criticism or review,
as permitted under the Copyright Act 1968, no part of this book may be reproduced
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Society for HIV Medicine.
Effort has been made to get permission from copyright owners for use of copyright
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appropriately capitalised. ASHM cannot attest to the accuracy of this information.
Use of a term in this book should not be regarded as affecting the validity of
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Although every effort has been made to ensure that drug doses and other
information are presented accurately in this publication, the ultimate responsibility
rests with the prescribing clinician. For detailed prescribing information or instructions
on the use of any product described herein, please consult the prescribing
information issued by the manufacturer.
Contents
Acknowledgments 4
Preface 6
Introduction to HIV and viral hepatitis
Chapter 1 HIV, HBV, HCV: similarities and differences 9
Joe Sasadeusz, Stephen Locarnini, Michael Kidd
Risk assessment and diagnosis
Chapter 2 Might this patient be positive? Epidemiology and transmission 17
Nicholas Medland, Gregory Dore, Andrew Grulich, David Bradford, Daniel Madeddu
Chapter 3 Talking with the patient: risk assessment and history-taking 24
Sarah Huffam, Paul Haber, Jack Wallace
Chapter 4 Exposure and acute HIV infection 30
Jonathan Anderson, John McAllister, Jon Willis, Phillip Keen,
Ronald McCoy, Andrew Grulich
Chapter 5 Exposure and acute viral hepatitis 37
Jeffery Post, Ingrid van Beek, George Marinos, Mary Burns
Chapter 6 Signs and symptoms of chronic HIV disease 46
Gary Rogers, Anne Mijch, Alan Brotherton
Chapter 7 Signs and symptoms of chronic viral hepatitis 54
Moira Sim, Wendy Cheng, Gregory Dore, Kelly Beers
Chapter 8 Talking about testing: pre-test and post-test counselling 63
Paul Andrews, Katharine Fethers, Ronald McCoy, Paul Harvey, Jenean Spencer
Management in the primary care setting
Chapter 9 Primary care management of HIV disease 71
David Orth, Jennifer Hoy, John Patten, Warren Fitzgerald, Anthony Allworth
Chapter 10 Primary care management of chronic viral hepatitis 84
Robert Feller, Simone Strasser, Jeff Ward, Gillian Deakin
Chapter 11 Palliative care 96
Brian McDonald, Michael Bramwell, Norman Roth, David Menadue
Professional issues
Chapter 12 Standard precautions and infection control 102
Nicholas Demediuk, Steve Wesselingh
Chapter 13 Legal responsibilities 107
Marilyn McMurchie, David Puls, Paul Nisselle, Anurag Kanwar
Chapter 14 Contact and referral information 114
Appendices
Appendix 1 Patient information Natural history and transmission of HIV 120
Appendix 2 Patient information Natural history and transmission of HBV 121
Appendix 3 Patient information Natural history and transmission of HCV 122
Appendix 4 Safe injecting and cleaning injecting equipment 123
Glossary 125
Index 127
Editors
Gregory Dore, Andrew Grulich, Michael Kidd, Jennifer Hoy, Ronald McCoy, Anne Mijch, and Simone Strasser.
Writers
Anthony Allworth; Jonathon Anderson; Paul Andrews; Kelly Beers; David Bradford; Michael Bramwell;
Alan Brotherton; Mary Burns; Wendy Cheng; Gillian Deakin; Nicholas Demediuk; Gregory Dore; Robert Feller;
Katherine Fethers; Warren Fitzgerald; Andrew Grulich; Paul Haber; Paul Harvey; Jennifer Hoy; Sarah Huffam;
Phillip Keen; Michael Kidd; Anurag Kunwar; Stephen Locarnini; John McAllister; Daniel Madeddu;
George Marinos; Ronald McCoy; Brian McDonald; Marilyn McMurchie; Nicholas Medland; David Menadue;
Anne Mijch; Paul Nisselle; David Orth; John Patten; Jeffery Post; David Puls; Gary Rogers; Norman Roth;
Joe Sasadeusz; Moira Sim; Jenean Spencer; Simone Strasser; Ingrid van Beek; Jack Wallace; Jeff Ward;
Steve Wesselingh; Jon Willis.
Reviewers
Melissa Bagatella (South Western Sydney Area Health Service, NSW); Laura Baird (Western Sydney Area
Health Service, NSW); Simon Benson (The Nicholson Street Clinic, Footscray, Vic); Frank Bowden (Gilmore
Clinic, Canberra Hospital, ACT); Di Bridger (James St Doctor, Hamilton, NSW); David Buchanan (Forbes
Chambers, Sydney, NSW); Ric Chaney (Boronia Medical Group, Mt Lawley, WA); John Chuah (Gold Coast
Sexual Health Clinic, QLD); Levinia Crooks (ASHM); John Cumming (AIDS Council of NSW); John Daniels,
Aboriginal Medical Service NSW); Liz Dax (National Serology Reference Laboratory Australia, Fitzroy, Vic);
William Donohue (SA Hepatitis C Council); Robyn Donellan (Prince of Wales Hospital, Sydney, NSW);
Heather Dowd (Western Region Health Centre, Melbourne, Vic); Katherine Fethers (Clinic 34, Alice Springs
Hospital, NT); Mary Foley (Leichhardt Womens Health Centre, NSW); Julie Garrard (Calvary Hospital, Sydney,
NSW); Louise Goggin (locum GP); Paul Harvey (Hepatitis C Council of NSW); Ken Hazelton (Dalton St Practice,
Orange, NSW); Margaret Hellard (Integrated Care, Monash University, Vic); Mark Kelly (Albion Street Centre,
NSW); Leighan Kerr (Ankali, NSW); Michelle Kosky (Consumers Health Forum, WA); Gai Lemon (QLD Hepatitis
C Council); Linda Mann (Leichhardt Family Practice, NSW ); Tony Maynard (ASHM); Lisa McCann (Sydney
Sexual Health Centre, NSW); Bob Milstein (Corrs, Vic); Dean Murphy (Australian Federation of AIDS
Organisations, NSW); Michael Noel (Wentworth Area Palliative Service, Nepean Hospital, NSW);
Anne Preston-Thomas (Ngaanyatjarra Health, Alice Springs, NT); Timothy Read (Melbourne Sexual Health
Centre, Vic); Suzanne Roche (Royal Prince Alfred Hospital, Camperdown, NSW); Miranda Sandars (North
Ivanhoe Medical Centre, Vic); David Thorne (St John of God Hospital, Perth, WA); Jack Wallace (Australian
Hepatitis Council, ACT); Chris Ward (Australian Federation of AIDS Organisations, NSW); Cassie Workman
(Ground Zero Medical Centre, Darlinghurst, NSW).
4 HIV/ Viral hepatitis a guide for primary care
Acknowledgments
ASHM Education Steering Committee
Alan Brotherton, Dean Murphy and Dermott Ryan (Australian Federation of AIDS Organisations);
Peter Canavan and Jo Watson (National Association of People Living with AIDS); Dianne Chambers (Royal
Australian College of General Practitioners); Michael Hand (Australian College of Rural & Remote Medicine);
Paula Henriksen, Diana Readshaw, Kate Jarvis, (HIV/AIDS and Hepatitis C Section, Department of Health and
Aged Care, DHAC); Jenny Hoy (Infectious Diseases Physician and ASHM Treatments Standing Committee);
Stephen Kent (Royal Australian College of Physicians/Australian Infectious Diseases Society); Tony Maynard,
Phillip Godwin, Julie Letts, Edward Reis, Levinia Crooks (ASHM); Anne Mijch (Infectious Diseases Physician
and ASHM Hepatitis C Standing Committee); Simone Strasser (Australian Liver Association/
Gastroenterological Society of Australia); Jack Wallace (Australian Hepatitis Council).
ASHM staff
Vanessa Sparrow (Project Coordinator); Megan Nicholson (Executive Editor); Julie Letts and Edward Reis
(Education Managers); Claire Koetsier, Heidi Nelson, Robert Booker, Greg Iverson, Michael Dwyer,
Lee Matthews (Administrative Ofcer); Carla Gorton (Information Services Manager); Phillip Godwin and
Tony Maynard (Education Ofcers), Levinia Crooks (ASHM Executive Ofcer).
Evaluation consultant
Lou McCallum
Additional sub-editors and proof-readers
Tim Badgery-Parker; Robert Booker; Wendy Bryant; Levinia Crooks; Vicky Fisher (2004 ed); Carla Gorton;
Megan Nicholson; Susie Prest; Vanessa Sparrow; Gary Wright, Helen Young.
Indexing
Libby Bessell-Browne, Megan Nicholson
Distribution and promotional consultant
Aldo Spina
Additional input
Chris Carmody (St Georges Hospital, NSW); Neil Cremasco (Tas Health Dept); John Daye (National
Association of People Living with AIDS); Simon Donohue and Kirsty Machon (Australian Federation of AIDS
Organisations); Fraser Drummond (NCHECR, 2004 ed); Jan Edwards (Australasian Society of Sexual Health
Physicians); Virginia Furner (Albion St Centre, Surry Hills, NSW); Judith Jones (Victorium Consortium);
Stuart Loveday (Hepatitis Council of NSW) Annie Madden (Australian Intravenous League); Gail Matthews
(NCHECR, 2004 ed); Philip Melling (NSW Infection Control Resource Centre, 2004 ed); Katherine Montieny
(WA Health Dept); Kim Petersen (SA Health Dept); Jackie Richmond (St. Vincents Hospital, Vic); Katrina Scott
(ACT Health Dept); Margaret Scott; Robert Scott (Australian Haemophilia Foundation); Bill Sievert (Australian
Liver Association/ Gastroenterological Society of Australia); Helen Taylor and Jo Holahan (Albion Street Centre);
Maggy Tomkins (Albion Street Centre, 2004 ed); Owen Westacott (NSW Health); Carol Whittaker and
Sue Mason (Central Sydney Area Health Service); Helen Williams (Queensland Health Dept).
HIV/ Viral hepatitis a guide for primary care 5
Preface
HIV/Viral hepatitis: a guide for primary care was conceived as a resource to provide general
practitioners and other interested clinicians and health care workers with an introduction to
HIV and viral hepatitis. The aim has been to produce a practical manual for risk assessment,
testing, diagnosis and basic principles of management of HIV and viral hepatitis, by review-
ing epidemiology, transmission, virology, history-taking, signs and symptoms, assessment
and primary care management of these chronic viral conditions.
The primary audience for this monograph is intended to be clinicians who test for HIV
and viral hepatitis and those who provide non-specialist care for infected patients.
Physicians, medical students, nurses, allied health professionals, as well as individuals with a
specic interest in these conditions, may also nd HIV/Viral hepatitis useful.
HIV/Viral hepatitis elucidates key differences and similarities in the assessment, diagnosis
and management of infections due to HIV, hepatitis B virus (HBV) and hepatitis C virus
(HCV). The second edition of the monograph builds on the rst, by utilising its strengths,
and updating information in many of the chapters. Risk assessment and testing for HIV,
HBV and HCV are often conducted together, because their patterns of transmission overlap.
There also may be overlapping clinical management issues, for example in relation to sexu-
ally transmissible infections, management of fatigue or of other symptoms associated with
chronic viral infections or patients with drug and alcohol dependence. In addition, the stig-
ma associated with infection with one or more of these viruses has a bearing on psychosocial
and legal issues.
The incorporation of viral hepatitis into an ASHM publication was a substantial change
of direction. It reects the trend in public policy and medical practice towards locating
HIV/AIDS within the broader public and sexual health context. Also it utilises the partner-
ship model established for the management of HIV infection within the context of hepatitis
C. Maximising the health of infected people through a range of interventions at the primary
care level is a key focus of HIV/Viral hepatitis, in line with the priorities delineated in the
National Hepatitis C Strategy and the National HIV/AIDS Strategy. The need for a collabo-
rative, shared care relationship between primary care clinicians and specialists is a central
theme. With the increasing complexity of clinical management, a productive shared care
model of care ensures best practice for the patient while maintaining medical standards and
legal requirements in relation to diagnosis, management and referral of patients. It is hoped
that HIV/Viral hepatitis will facilitate closer working relationships between general practi-
tioners, specialists and other health service providers in the areas of HIV, viral hepatitis and
sexual health generally.
Many organisations and individuals have contributed to the production of the rst and
this revised, second edition of this monograph. On behalf of ASHM, we would like to
acknowledge the input of the Royal Australian College of General Practitioners, the
Gastroenterological Society of Australia (GESA)/ Australian Liver Association, the Royal
College of Physicians, the Australian College of Rural and Remote Medicine, the Australian
Federation of AIDS Organisations, the National Association of People Living with AIDS and
the Australian Hepatitis Council.
We would also like to acknowledge the tremendous contribution of the chapter authors:
Anthony Allworth; Jonathon Anderson; Paul Andrews; Kelly Beers; David Bradford; Michael
Bramwell; Alan Brotherton; Mary Burns; Wendy Cheng; Gillian Deakin; Nicholas
Demediuk; Gregory Dore; Robert Feller; Katherine Fethers; Warren Fitzgerald; Andrew
Grulich; Paul Haber; Paul Harvey; Jennifer Hoy; Sarah Huffam; Phillip Keen; Michael Kidd;
Anurag Kunwar; Stephen Locarnini; John McAllister; Daniel Madeddu; George Marinos;
Ronald McCoy; Brian McDonald; Marilyn McMurchie; Nicholas Medland; David
Menadue; Anne Mijch; Paul Nisselle; David Orth; John Patten; Jeffery Post; David Puls; Gary
Rogers; Norman Roth; Joe Sasadeusz; Moira Sim; Jenean Spencer; Simone Strasser; Ingrid
van Beek; Jack Wallace; Jeff Ward; Steve Wesselingh; Jon Willis.
Authors and reviewers gave time and energy to this project in the context of busy prac-
tices and heavy workloads, and their demonstrated commitment to medical education
deserves considerable recognition. Thanks to the many other individuals (page 5) who con-
tributed ideas and information to the project.
We would also like to acknowledge the contribution of Jenny Hoys co-editors Greg Dore,
Andrew Grulich, Michael Kidd, Ron McCoy, Anne Mijch and Simone Strasser, and ASHM
project staff Julie Letts, Megan Nicholson, Vanessa Sparrow, and Vicky Fisher who has over-
seen the second edition of this monograph.
The rst edition of HIV/Viral hepatitis was funded by the Commonwealth Department of
Health and Aged Care (DHAC) and the Australian National Council on AIDS, Hepatitis C
and Related Diseases (ANCAHRD) through the ASHM National HIV Education Program
and the ASHM National Hepatitis C Education Program. The second edition was funded by
the Commonwealth Department of Health and Ageing.
Jennifer Hoy Elizabeth Dax
Chair, Treatments Committee, ASHM ASHM President
Melbourne, April 2004 Melbourne, April 2004
1
HIV, HBV, HCV: similarities and differences
Joe Sasadeusz Head of Medical Virology, Victorian Infectious Diseases Service, Royal Melbourne Hospital,
Victoria.
Stephen Locarnini Head of Research and Development, Victorian Infectious Diseases Reference Laboratory,
Melbourne, Victoria.
Michael Kidd Head of the Department of General Practice, The University of Sydney, New South Wales.
Introduction
The three major blood-borne viruses (BBV),
human immunodeciency virus (HIV), hepatitis B
virus (HBV) and hepatitis C virus (HCV), are
members of different virus families but share one
thing in common: their major mode of transmis-
sion is via blood or bodily uids. This chapter
compares the three agents, specically focusing on
their virology, transmission, pathogenesis and
natural history. It also provides an introduction to
the principles of therapy and discusses the effects
of therapy on the natural history of each of these
infections.
Virology
HIV
The manifestations of HIV were rst apparent in
the early 1980s when an epidemic of unexplained
cases of immunodeciency was recognised in the
western world. Evidence suggested the cause to be
a transmissible agent, and in 1984 the agent was
conrmed to be a retrovirus now known as human
immunodeciency virus (HIV). Human infection
may date back to the early part of the twentieth
century and the virus may have originally been
transmitted zoonotically to humans from primates
in Africa.
HIV is a single-stranded ribonucleic acid (RNA)
virus. It has an outer envelope that surrounds two
copies of single-stranded RNA as well as a number
of viral proteins. From its outer envelope protrudes
the 120 glycoprotein (gp 120). The HIV replication
cycle commences when gp120 attaches to the CD4
receptor and the chemokine co-receptor CCR5.
(These receptors are expressed on the surface of
the CD4 lymphocyte, the cell HIV predominantly
infects.) Attachment precipitates the fusion of the
Key points
Human immunodeciency virus (HIV), hepatitis B virus (HBV)
and hepatitis C virus (HCV) are distinct viruses with different
epidemiological proles, modes of transmission, natural
histories and treatments.
All three viruses lead to chronic infection in many infected
individuals and are characterised by hypermutability and
quasispecies.
HIV is transmitted through sexual contact, blood-to-blood
contact and mother-to-child transmission. Without treatment,
most infected individuals develop severe immune deciency
within ten years. Combination antiretroviral therapy has
transformed the course of the disease, extending the life
expectancy of infected individuals by many years.
HBV is transmitted through mucous membrane contact
(including unprotected sexual contact), blood-to-blood contact,
mother-to-child transmission and intrafamilial transmission.
A safe and effective vaccine against HBV is available. The age
of infection is crucial in determining the natural history of HBV.
For people who develop chronic active hepatitis B, treatment
is effective in a substantial minority of patients. Chronic active
hepatitis B may progress to cirrhosis and hepatocellular
carcinoma.
HCV is transmitted primarily through blood-to-blood contact.
The sharing of equipment during injecting drug use is the most
common mode of transmission in Australia. A minority of
people clear HCV from the body but the majority develop a
chronic infection. Some chronically infected individuals will
develop symptoms such as fatigue and nausea. A small
proportion of individuals will progress to liver failure or
hepatocellular carcinoma. Combination therapy may be
effective, although HCV genotype signicantly inuences
response to treatment.
1 HIV, HBV, HCV: similarities and differences
membranes of virus and cell via the HIV envelope
glycoprotein gp41, allowing the virus to enter the
cell. The RNA then undergoes reverse transcription,
a process whereby RNA is converted to deoxyri-
bonucleic acid, or DNA, using the viral-encoded
reverse transcriptase. The resulting viral DNA,
called the provirus, migrates to the nucleus and
integrates into the host chromosome. The provirus
acts as a template to allow production of messen-
ger RNA to produce the components of new virus
particles, including the RNA genome of new viri-
ons. The viral proteins are processed and cleaved
by another virus-specic enzyme known as HIV
protease. Viral proteins and RNA are then assem-
bled and bud from the cell membrane, forming
mature HIV particles that can infect other cells.
Some of the CD4 cells are irreparably damaged by
HIV infection. Premature cell death of damaged
CD4 cells in part contributes to the immunosup-
pression characteristic of advanced HIV disease.
1
HBV
HBV is a non-cytopathic virus and contains a
partially double-stranded DNA genome. This
virus predominantly infects hepatocytes and
belongs to the hepadnavirus family. HBV has an
outer envelope containing surface antigen (HBsAg)
and a core containing core antigen (HBcAg).
Excess HBsAg is produced as sub-viral particles
which circulate in the blood and permit
convenient serological diagnosis of HBV. The
core contains the genomic DNA as well as the
viral-encoded DNA polymerase, which is detected
in liver tissue. HBV also produces e antigen or
HBeAg, which is secreted into the blood and is
detected by serological assay. The presence of
circulating HBeAg and serum HBV DNA is
indicative of ongoing viral replication and
increased infectivity. Resolution of HBV infection
is accompanied by clearance of HBeAg and
HBsAg and seroconversion to anti-HBe-positive
(anti-HBe+) and anti-HBs-positive (anti-HBs+).
Soon after entering the hepatocyte, the
genomic DNA is converted in the nucleus to a
form known as supercoiled or covalently closed
circular (ccc) DNA. This serves as a template to
yield two types of RNA: a pregenomic RNA
that ultimately undergoes reverse transcription
to yield DNA for progeny virus and messenger
RNA for structural proteins. The former is
assembled into mature virions that are then
released from the cell. In long-term, chronic
infection, HBV DNA may integrate into the
host cell genome but integration is typically
incomplete and a full lifecycle cannot occur
from these integrated sequences. Viral
integration does play a role in the development
of hepatocellular carcinoma, especially in the
setting of cirrhosis. Supercoiled HBV DNA in
the liver cell nucleus is long-lived and resistant
to all current antiviral therapies, resulting in
lifelong chronic infection.
2
HCV
HCV is a single-stranded, enveloped RNA virus
belonging to the avivirus family. It causes most
cases of what was previously known as non-A,
non-B hepatitis. HCV was discovered when
infected serum was injected into a number of
chimpanzees, whose sera were then used to identify
a clone that reacted with an infected serum panel
from patients with non-A, non-B hepatitis. This
finding ultimately formed the basis of the first
antibody test for detection of HCV. The virus has
not yet been cultivated in cell culture systems.
The HCV replication cycle has been partially
elucidated. The viral receptor has not been
conclusively demonstrated on the hepatocyte.
Following infection of the hepatocyte and inter-
nalisation of the virus, HCV RNA is translated by
the host cell ribosomes to produce a large viral
polyprotein, which is cleaved and processed by
both host cellular and virus-specic (NS-2 and
NS-3) enzymes. The viral polymerase/replicase
(NS-5B) copies the viral RNA in the cytoplasm
and, as soon as a pool of progeny RNA molecules
and core proteins is present, assembly of the
nucleocapsids occurs. Mature HCV virions then
develop and bud through the plasma membrane.
Quasispecies and hypermutability
The replicase enzymes of all three viruses, the
HIV reverse transcriptase, the HBV DNA
polymerase and the HCV RNA polymerase, are
hypermutatable. Mutation, particularly under
immunological and/or therapeutic pressure, leads
to the presence in a given individual of a number
of closely related, but genetically distinct, viral
variants known as quasispecies. The emergence
of quasispecies is the likely reason why infection
with these viruses results in chronic infection in
most individuals despite a host immune response.
Each one of the virus-specic enzymes previously
discussed is the focus of intense research to
develop potent and selective inhibitors of key
viral functions, which could result in signicant
gains in managing the health of people persistently
infected with these viruses.
3
Transmission
While each virus has distinct transmission patterns,
HIV, HBV and HCV can all be transmitted
parenterally through the sharing of injecting
equipment, needle-stick injuries, or piercing and
tattooing with contaminated equipment. On the
other hand, efficiency of sexual transmission
differs markedly between viruses.
HIV
HIV is predominantly transmitted sexually, with
efciency being greatest through receptive anal
intercourse. In Australia, transmission is most
commonly seen in homosexual men, whereas in
developing countries, especially in Africa, HIV is
predominantly acquired through vaginal inter-
course. Transmission through injecting drug use is
uncommon in Australia, accounting for 4% of
HIV cases, but is particularly prevalent in parts of
Europe and Asia (including countries of the
former Soviet Union) and the United States.
Transmission by blood products largely occurred
before the introduction of antibody screening in
1985 in Australia and was responsible for the
high incidence of HIV among multiply-transfused
people, such as in haemophilia; it is now exceed-
ingly rare in countries where blood is screened.
Transmission by needle-stick injury occurs in
0.3% of exposures from HIV-infected individuals.
Perinatal transmission occurs in 2045% of
infants born to infected mothers, but this can be
reduced to less than 5% with the administration
of antiretroviral therapy during pregnancy, labour
and after delivery, and other interventions, such as
caesarean section and avoidance of breast-feeding.
4
In Australia there have been 19,674 new diag-
noses of HIV infection, with 9,083 cases of AIDS
by the end of 2002 and 6,272 cases of AIDS-
related deaths.
5
HBV
Most HBV cases result from perinatal transmission,
which accounts for high prevalence in people
from endemic countries, particularly China and
South East Asian and Pacic nations. Transmission
is effectively prevented by HBV vaccination and
administration of hepatitis B immunoglobulin
(HBIG) to newborns of HBsAg+ women, but
such programs are not currently available in
many developing countries where most cases
occur. Among adults, HBV transmission is pre-
dominantly via sexual contact and injecting drug
use. In Australia, the overall prevalence of the
HBV carrier state has been estimated to be 160,000
to 200,000. The risk of transmission by percuta-
neous exposure such as a needle-stick injury is
approximately 30% if the carrier has replicative
disease (HBV DNA+ by hybridization assay or
HBsAg+), compared with 3% for carriers with
non-replicative disease (that is, people without
HBeAg or HBV DNA).
2
HCV
HCV transmission is predominantly parenteral.
The most common mode of transmission in
Australia remains injecting drug use, which
is responsible for approximately 80% of the
estimated 225,000 prevalent cases nationally and
reported as the predominant risk factor in over
90% of the estimated 16,000 annual incident
cases.
6
Among particular immigrant populations,
poor infection-control practices during procedures
such as vaccination (European- and Asian-
acquired) and chemoprophylaxis programs for
schistosomiasis (Egyptian-acquired) may have
been responsible for many cases. The role of sexu-
al transmission, if any, is still controversial. If sex-
ual transmission of HCV does occur, it is at a very
low level that makes it inappropriate to routinely
recommend safe sex among long-term monoga-
mous couples. Sexual transmission is likely to be
more efcient, however, where there is HIV coin-
fection and high HCV viral load. Risk of sexual
transmission may also be increased when blood is
present in the genital tract, such as during men-
struation. Perinatal transmission occurs in
approximately 5% of deliveries, although this
may be higher in women who have HIV coinfec-
tion or high levels of viraemia. Elective caesarean
section in women with HIV/HCV coinfection is
usually advocated, although its role in reducing
perinatal transmission in women with HCV
monoinfection is unclear.
7,8
Natural history
HIV
Following inoculation with HIV, there is a period
of high-level viraemia associated with a reduction
in the CD4 cell count. A host immune response
then develops, partially controlling viral
replication, but is unable to clear HIV from the
body. A substantial proportion of patients
(proportions in recent reports range from 50% to
92%) suffer a mononucleosis-like seroconversion
illness characterised by fever, pharyngitis,
lymphadenopathy, rash, splenomegaly and aseptic
meningitis. Other HIV-infected patients are
asymptomatic or suffer a more non-specific
illness. These acute-phase effects then resolve as
the immune system mounts an antiviral response
that causes the viral load to decrease markedly.
Simultaneously, there is a rebound increase in
CD4 cell count to near baseline levels and the
patient enters a period of clinical latency,
although very high levels of viral replication
continue, especially in the lymphoid compartment.
The plasma HIV RNA plateaus to a constant
level of viraemia known as the virological set
point. The level of this set point is the best
available predictor of progression to AIDS. If left
untreated, the patient experiences a gradual
decline in CD4 cell count and, after a mean of
ten years, develops AIDS with the onset of
opportunistic infections or malignancies. At this
time the CD4 cell count has usually fallen below
200 cells/l and the patient is severely
immunocompromised (Figure 1.1).
1,9
HBV
HBV, by contrast, is almost exclusively an immune-
mediated disease. The outcome of infection is
largely determined by the age at infection, which
relates to the maturity of the immune response. In
endemic countries where infection occurs during
birth (perinatal infection) or in early childhood
(early horizontal infection), over 90% of HBV
transmissions will become chronic (as dened by
a persistence of HBsAg for more than six months),
although clinical acute hepatitis rarely occurs. If,
however, an individual is infected as an adult,
chronic infection will occur in less than 5% of
individuals, although almost half will manifest
clinical features of acute hepatitis.
The natural history of chronic HBV infection
has been dened by stages of immune response.
Initially patients have no immune response to the
virus and are said to be in the immunotolerant
phase. At this time, they have normal liver function
despite high levels of HBV DNA and detectable
HBeAg, indicating active viral replication. Later
in life, usually in the second to fourth decade, the
immune system is triggered to attack the virus-
infected hepatocyte and a period of immune clear-
ance ensues, whereby patients demonstrate ares
of elevated serum aminotransferase levels with
histological evidence of active hepatitis.
If these ares persist for too long or are sub-
stantial, the patient may ultimately develop cir-
rhosis and liver failure. About 2540% of long-
term carriers will die of cirrhosis or hepatocellular
carcinoma (HCC) (Figure 1.2). However, if these
FIGURE 1.1 The various stages of HIV infection depicting the development of different opportunistic infections with advanced
immunodeciency and the impact of antiretroviral therapy on CD4 cell count recovery.
HIV NATURAL HISTORY
1000
500
200
10 weeks 5 years 10 years 12 years
Fever
Myalgia
Rash
Pharyngitis
Adenopathy
Mouth ulcers
Asymptomatic
Thrombocytopenia
PCP, KS
MAC, CMV
Minor infections
Skin conditions
Fever
Weight loss
TB
Pneumonia
Toxoplasmosis
Cryptosporidiosis
Lymphoma (NHL)
Antiretroviral therapy
Primary Early Intermediate Late
CD4
cell count
(cells/l)
Time
immune-based clearances are successful, the
patient will demonstrate an HBeAg seroconver-
sion to anti-HBe, have undetectable HBV DNA
by hybridisation assay and show normalisation of
serum aminotransferase levels with associated
improvement of liver histology. The HBV carrier
then enters into the latent phase with an improved
long-term prognosis (Figure 1.2).
Occasionally, under the pressure of immune-
mediated flares, HBV mutants are selected.
These so-called precore (or HBeAg-negative)
mutants fail to secrete HBeAg protein but still
replicate, as evidenced by detectable HBV DNA
in serum and elevated serum aminotransferase
levels. HBeAg-negative infection is particularly
prevalent in certain geographical areas such as
around the Mediterranean basin and in South
East and northern Asia. In Australia, migrants
from these regions are frequently infected with
such variants.
2
FIGURE 1.2 Demonstrates the three phases of infection in a person from an endemic area.
* Cirrhosis may develop during the period of attempted immune clearance.
** Antiviral therapy increases the likelihood of HBeAg to anti-HBe seroconversion.
Active disease may occur despite loss of HBeAg.
Treatment may induce
seroconversion and enhance
clearance.**
Age (years) 0 10 20 30 40 50
HBV NATURAL HISTORY
Spontaneous
seroconversion
HBeAg
Normal
Chronic hepatitis*
Prolonged clearance =
greater risk of cirrhosis or HCC.
Serology
HBV DNA
ALT
Pathology
Phase
Minimal histologic change or
cirrhosis / HCC**
III - Residual integrated II - Clearance
I - Immunotolerant
Anti-HBe
HCV
Unlike HBV, the immune response generated in
adults newly infected with hepatitis C is usually
inadequate to effectively control viral replication.
As a consequence, the majority of acute infections
progress to chronic infection, dened as a positive
HCV RNA in serum six months after the estimat-
ed date of infection. The proportion of people
estimated to clear acute hepatitis C varies from
between 25 to 40% and clearance occurs more
frequently in patients who are symptomatic or
who become jaundiced. Understanding of the nat-
ural history of chronic hepatitis C infection has
improved in recent years with the realisation that
fewer people progress to cirrhosis than was origi-
nally estimated. Models based on large longitudi-
nal community-based cohorts estimate the risk of
progression to cirrhosis to be 7% at 20 years and
20% at 40 years of infection.
10
Estimates of
FIGURE 1.3 The natural history of hepatitis C infection and the impact of successful therapy on infection.
HCV PROGNOSIS AND PROGRESSION
HCV infection
Good prognosis
1-5% HCC, 2-5% liver failure
30-40% normal ALT 60-70% abnormal ALT
10-20% cirrhosis
Sustained response to IFN + RBV
75% chronic 25% spontaneous resolution ?Cure
hepatitisC related mortality are 1 and 4 % at 20
and 40 years respectively.
10
Despite this, an
increasing burden of advanced liver disease is
anticipated within Australia over the future years,
with between 15, 000 and 20,000 cases of cirrho-
sis by the year 2010.
Factors associated with an accelerated risk of
progression include older age at infection, male
sex, heavy alcohol intake, coinfection with HBV
and HIV and possibly obesity, linked to the pres-
ence of steatosis (fatty liver) on biopsy. The risk of
liver failure in people with compensated cirrhosis
is around 4-5% per year and the risk of hepatoma
around 1-3% per year in Australia.
People who have chronic hepatitis C and nor-
mal liver function tests generally have very low
rates of brosis progression. At present the major-
ity of these patients are not routinely offered HCV
therapy and are treated only in the context of clin-
ical trials.
Coinfection
Multiple blood-borne viral infections in the same
individual can markedly alter the natural history
of disease. For example, HBV has no adverse
effect on HIV or the development of AIDS, but HIV
does inuence HBV and can be associated with
accelerated development of cirrhosis and liver fail-
ure. Individuals with HIV and HCV coinfection
have higher HCV viral loads and a more rapid
course to end-stage liver disease.
This has been demonstrated by the correlation
between declining CD4 cell counts and the
increasing percentage of HCV-related hospital
admissions and deaths among people with
HIV/HCV coinfection.
11
Therapy
HIV
The course of HIV has been drastically altered by
the introduction of highly active antiretroviral ther-
apy (HAART or combination antiretroviral thera-
py). This therapy usually consists of a combination
of at least three drugs from two or three of the dif-
ferent classes of antiretrovirals: the nucleoside ana-
logue reverse transcriptase inhibitors (NRTIs), the
non-nucleoside reverse transcriptase inhibitors
(NNRTIs) and protease inhibitors (PIs). A combi-
nation of three agents, usually two NRTIs com-
bined with either an NNRTI or PI, is administered
when the CD4 cell count falls below a certain
threshhold.
Although the optimal time to commence thera-
py has not been established, Australian and inter-
national guidelines recommend that treatment
should be considered when the CD4 count is
between 200350 cells/mm
3
or the HIV viral load
is above 55,000 copies/ml. Individualised deci-
sions should take into account the patients readi-
ness to start therapy, the baseline CD4 cell count
and HIV RNA level and the potential risks and
benets of treatment. Combination antiretroviral
therapy is very potent in reducing viral load and
delaying drug resistance, and has resulted in a dra-
matic reduction in mortality and increased life
expectancy in HIV-infected individuals. The life
expectancy of people with a CD4 cell count over
200 cells/l is projected to be in excess of 30 years.
This success has meant that HIV infection may
become a chronic manageable disease. Immune-
based therapies, such as interleukin-2 and therapeutic
vaccination, are also under investigation.
The aim of therapy for HIV infection is to
sustain an undetectable viral load, which is
achievable in approximately 5060% of patients,
and to produce immune restitution. Immuno-
logical benet may be modest (CD4 cell counts
frequently remain below normal levels) but often
occur in individuals who fail to achieve full viro-
logical suppression.
At present we do not know the long-term dura-
bility of the response in those who achieve viral
control or whether drug resistance and loss of ef-
cacy will ultimately emerge. Most of these drugs do
have signicant side-effects and require complex
dosing schedules, making adherence (a major
determinant of resistance) an issue for concern.
Long-term survival of these patients also has
unmasked chronic drug toxicities, particularly
metabolic problems such as lipodystrophy and
lipoatrophy, hyperlipidaemia, insulin resistance
and hepatic mitochondrial toxicity.
12
HBV
Current therapy for chronic HBV infection
involves either alpha interferon (IFN) or lamivu-
dine and is only considered when a patient enters
the immune clearance phase, as the mechanism of
therapy is to augment the existing endogenous
immune response. The aim of therapy in an
HBeAg+ patient is to facilitate a durable serocon-
version to anti-HBe with resolution of liver
inammation (Figure 1.2). Interferon therapy for
46 months results in HBeAg seroconversion in
approximately 3040% of individuals but is asso-
ciated with signicant side-effects. Lamivudine for
12 months results in about 20% seroconversion
in patients who have greater than twice the upper
limit of normal serum alanine aminotransferase
(ALT) level, with even higher rates (around 50%)
if the serum ALT level exceeds ve times the upper
limit of normal. Seroconversion increases linearly
for up to three years, although at a cost of viral
resistance, which reaches at least 50% at this
time. The overall resistance rate appears to be
20% per year treated. The treatment of HBeAg-
negative infection is problematic and should
probably be undertaken only if there is aggressive
liver disease. Therapy probably needs to be life-
long, as withdrawal of therapy is associated with
rebound viraemia and signicant hepatitis ares.
Ultimately, chronic HBV, like HIV, may be best
treated with combination therapy.
11,12,13
Progression to end-stage liver disease may man-
date liver transplantation, although aggressive rein-
fection of the graft is problematic and necessitates
the use of preventative strategies including antiviral
therapy and HBV immunoglobulin.
HCV
Assessment of the need for therapy usually requires
liver biopsy unless patients have a contraindication
such as coagulopathy. This is due to the inability of
non-invasive investigations to accurately assess dis-
ease activity. Therapy is usually given to patients
with brosis and/or moderate inammation on
biopsy, as per S100 treatment guidelines.
Treatment for HCV has markedly improved in
recent years. The combination of ribavirin with the
newer form of interferon known as pegylated-inter-
feron or PEG-interferon has greatly improved
response rates compared to interferon-
alfa monotherapy, and this combination is now
considered standard of care. Pegylated interferon is
2 Lee WM. Hepatitis B infection. N Engl J Med
1997;337:1733-1745.
3 The National Institutes of Health. Consensus
Development Conference: Management of hepatitis
C. Hepatology (supplement 1) 1997.
4 Dorenbaum A, for the PACTG 316 Study Team. Report
of results of PACTG 316: an international phase III trial of
the standard antiretroviral (ARV) prophylaxis plus
nevirapine for prevention of perinatal HIV transmission.
Program and Abstracts of the 8th Conference on
Retroviruses and Opportunistic Infections: 2001 Feb 4-8;
Chicago, USA. Abstract LB7.
5 National Centre in HIV Epidemiology and Clinical
Research. HIV/AIDS, viral hepatitis and sexually
transmissible infections in Australia, Australian HIV
Surveillance Report. 2003.
6 Law MG, Dore GJ, Bath N, et al Modelling hepatitis C
virus incidence, prevalence and long-term sequelae in
Australia, 2001. Int J Epid 2003; 32:717-724.
7 MacDonald M, Crofts N and Kaldor J. Transmission of
hepatitis C virus: rates, routes, and cofactors.
Epidemiol Rev 1996;18:137-146.
8 Crofts N, Jolley D, Kaldor J, van Beek I, Wodak A.
Epidemiology of hepatitis C virus infection among
injecting drug users in Australia. J Epidemiol
Community Health 1997;51:692-697.
9 Chakraborty R and Rowland-Jones S. The
pathogenesis of HIV disease. Journal of HIV Therapy
1999;4:2-8.
10 Dore GJ, Freemen AJ, Law M, Kaldor JM Is severe
liver disease a common outcome for people with chronic
hepatitis C? Journal of Gastroenterology and
Hepatology 2002;17, 423-430.
11 Dieterich D. Hepatitis C virus and human
immmunodeciency virus: clinical issues in
coinfection. Am J Med 1999;107:79S-84S.
12 International AIDS Society-USA Panel. Antiretroviral
therapy in adults: Updated recommendations of the
International AIDS Society-USA Panel. JAMA
2000;283:381-390.
13 Hoofnagle JH and Di Bisceglie AM. The treatment of
chronic viral hepatitis. N Engl J Med 1997;336:347-
356.
14 Torresi J and Locarnini S. Antiviral chemotherapy for
the treatment of hepatitis B virus infection.
Gastroenterology 2000;118:S83-103.
15 Shaw T and Locarnini S. Combination chemotherapy
for hepatitis B virus: the nal solution? Hepatology
2000;32:430-432.
16 Manns MP, McHutchison JG, Gordon SC, et al.
Peginterferon alfa-2b plus ribavirin compared with
interferon alfa-2b plus ribavirin for initial treatment of
chronic hepatitis C: a randomized trial. Lancet 2001,
358: 958-965
17 Fried MW, Shiffman ML, Reddy R, et al. Peginterferon
alfa-2a plus ribavirin for chronic hepatitis C virus
infection. N Engl J Med 2002, 347 : 975-982
18 Hadziyannis SJ, Sette H, Morgan TR, et al for the
PEGASYS International Study Group. Peginterferon-
alfa 2a and ribavirin combination therapy in chronic
hepatitis C. A randomized study of treatment duration
and ribavirin dose. Annals of Internal Medicine,
2004;140: 346-355
19 Pianko S and McHutchison JG. Treatment of hepatitis
C with interferon and ribavirin. J Gastroenterol Hepatol
2000;15:581-586.
produced through the attachment of a polyethylene
glycol (PEG) molecule to standard interferon. This
improves the pharmacokinetic properties of interfer-
on and allows for once-weekly dosing. Not only is
this new formulation more convenient to administer
but response rates are enhanced. Sustained virologi-
cal remission (SVR) is dened as the absence of HCV
RNA from serum six months after completion of
therapy and is inuenced by both HCV genotype
and HCV viral load.
SVRs with standard interferon/ribavirin combi-
nation are in the region of 35% for genotype 1 and
80% for genotype 2/3 . With pegylated interferon
there is a signicant improvement in genotype 1
response rates by approximately 10% to between 42
and 52%.
16,17,18
The anticipated SVR rate for geno-
type 2/3 patients remains very high at around 80%.
The duration of therapy required is also genotype
dependent with genotype 2/3 patients requiring only
6 months of therapy compared to 12 months of ther-
apy for genotype 1 patients. Response rates in cir-
rhotic patients are also markedly improved with
pegylated interferon therapy compared to standard
interferon therapy (SVR 43% versus 33%).
Once SVR has been achieved it is highly durable
with almost all (>95%) of patients remaining clear of
virus with extended follow-up.
End-stage liver disease due to HCV is now the
most common indication for liver transplantation
in Australia. Graft re-infection is almost universal
although disease progression is still relatively slow
in most cases.
3,19
Prevention
There is an effective and safe vaccine for HBV
which is currently being introduced into Australia
as a component of the universal vaccine program.
While this program takes effect, it is important to
offer vaccination to high-risk patients.
Unfortunately, technical difficulties associated
with vaccine development suggest that effective
vaccines for HIV and HCV are at least 510 years
away.
Prevention strategies based on public health
behaviour modication and harm minimisation
approaches have been effective in Australia and
elsewhere and remain the foundation of preven-
tion for individuals at risk of these viral infections.
References
1 Stewart G, (ed). Managing HIV. North Sydney:
Australasian Medical Publishing Company Ltd;
1997.
Patients with acute HIV, HCV or HBV infection
may present with symptoms (Chapters 4 and 5),
and diagnosis of HIV or viral hepatitis should be
considered in any febrile illness, particularly if there
is a possibility of recent exposure. When symptoms
of chronic infection do occur, they are often non-
specic (e.g. fatigue, myalgia and fevers).
Symptoms and signs of moderately advanced
HIV infection include weight loss, chronic
diarrhoea, fevers, lymphadenopathy, oral candidi-
asis, seborrheic dermatitis, herpes zoster, frequent
or severe recurrent oral or genital herpes and oral
hairy leukoplakia. Symptoms and signs of early
chronic viral HBV and HCV infection are more
non-specic and include intermittent or chronic
fatigue, abdominal discomfort, and headaches.
Symptoms and signs of more advanced chronic
viral hepatitis include the exanthemata of chronic
liver disease (palmar erythema, spider naevi),
2
Might this patient be positive?
Epidemiology and transmission
Nick Medland General Practitioner, The Centre Clinic, Victorian AIDS Council/Gay Mens Health Centre,
St Kilda, Victoria.
Andrew Grulich Epidemiologist and Public Health Physician, National Centre in HIV Epidemiology and Clinical
Research, Darlinghurst, New South Wales.
Greg Dore Epidemiologist and Infectious Diseases Physician, National Centre in HIV Epidemiology and
Clinical Research, Darlinghurst, New South Wales.
David Bradford Sexual Health Physician, Cairns Base Hospital, Queensland.
Daniel Madeddu HIV/AIDS Educator, Victorian AIDS Council/Gay Mens Health Centre, South Yarra, Victoria.
Key points
HIV and HBV are transmitted through sexual contact, as well
as blood-to-blood contact and from mother to child. HCV is
transmitted by blood-to-blood contact.
In Australia, the prevalence of HIV, HBV and HCV is high
among particular groups. However, risk exposure rather than
group membership should be the basis for risk assessment.
The decision to test should be based on an assessment of risk
as well as physical examination. Individuals may prefer not to
reveal a history of risk behaviour, and a low threshold for
testing should be maintained.
Individuals infected with a blood-borne virus who do not report
high-risk behaviours are more likely to present late and to
suffer resultant poor clinical outcomes.
Introduction
Early diagnosis is important for all treatable condi-
tions. Early identification of blood-borne viral
infections in particular can facilitate both treatment
and prevention. Therapy for HIV infection can
postpone immune damage and prevent develop-
ment of opportunistic infections and malignancies,
while improved therapies for HBV and HCV can
clear virus and improve clinical outcomes in some
individuals. In addition to providing the benets of
treatment, early diagnosis, accompanied by rele-
vant education, can help to reduce the rate of ongo-
ing transmission of HIV, HBV and HCV.
Diagnosis of each of these infections requires a
simple blood test. However, indications for testing
are frequently overlooked and opportunities for early
diagnosis are missed. The decision to test should be
based on a detailed history of risk behaviour as well
as a physical examination. It should always be borne
in mind that individuals may prefer to conceal a
history of risk behaviour. Consequently, a low
threshold for testing should be maintained.
Individuals infected with a blood-borne virus who
do not report high-risk behaviours are more likely
to present with advanced disease. Late presentation
has been associated with poor clinical outcomes,
particularly in relation to HBV and HIV.
Clinical assessment:
might the patient be positive?
The majority of patients chronically infected with
HIV, HBV or HCV are asymptomatic. The diag-
nosis relies on the clinician retaining an index of
suspicion in all clinical situations, and on a
thorough assessment of risk.
while decompensated cirrhosis (liver failure) is
associated with development of ascites,
splenomegaly and abdominal venous distension
(Chapters 6 and 7).
Risk assessment:
might this patient be positive?
Risk assessment is based on a thorough history of
the patients sexual practices, drug use, tattoos
and piercings and medical history relating to vac-
cination, use of blood products in Australia (prior
to 1985 for HIV and 1990 for HCV) and possible
medical exposure overseas. The history should be
taken in a manner that enables the patient to
discuss recent and remote risks and exposures
(Chapter 3). Whilst taking a complete history
may not be an option at every general practice
contact, it may be possible to accrue this informa-
tion over a period of time. Alternatively, the
patient may be offered a follow-up appointment
to allow risk assessment to be completed.
When faced with an individual who is an
identiable member of a high-risk group (e.g. an
openly gay man or an opiate-dependent drug
user), the possibility of infection with a blood-
borne virus is likely to suggest itself. However, as
transmission is actually linked to certain risk
behaviours, rather than group membership, it is
likely that considering the possibility of infection
with HIV, HBV or HCV only in persons from so-
called high-risk groups will lead to undetected
infections. Many individuals who are from such
high-risk groups remain at very low risk because
of the nature of their sexual or drug-use practices,
while individuals from perceived low-risk
groups may undertake high-risk behaviours.
A person may not provide truthful or accurate
information regarding risk behaviours for several
reasons including:
experience of discrimination within the health
system and from health care workers on the
basis of drug use or sexual behaviour;
non-acceptance of his/her own behaviours and
an inability to discuss these behaviours with
any other person, even a health professional;
the desire to disassociate from past risk
behaviours;
cultural shame and/or language barriers to
disclosure;
fear that condentiality will be breached.
A minority of individuals may not report high-
risk behaviour at all. They may simply have had
an unprotected heterosexual encounter (which
2 Might this patient be positive? Epidemiology and transmission
CASE STUDY 1
Clinical assessment: cough and fever may indicate
an HIV-related illness
Cough and fever
Jessica is a 37-year-old secretary who presents to her GP with a
recent onset of cough and fever. Brief chest examination is
unremarkable and she is prescribed ve days of amoxycillin. She
re-presents three weeks later with marked shortness of breath,
weakness and fatigue. Chest X-ray shows signs consistent with a
diffuse pneumonitis and she is admitted to hospital. Jessicas HIV
antibody test is positive (ELISA and Western Blot) and she has a
CD4 cell count of 25 cells/l and a HIV viral load of 500,000
copies/ml. Upon presumptive treatment for Pneumocystis carinii
pneumonia (PCP), the cough resolves and chest X-ray normalises.
Jessica is commenced on triple combination antiretroviral therapy
that she tolerates well. One year after presentation, she remains
well on antiretroviral therapy and PCP prophylaxis.
CASE STUDY 2
Risk assessment: non-disclosure of high-risk
sexual activity
Sexual risk activity
A 29-year-old garage mechanic attends his GP complaining of a
purulent urethral discharge. He seems open, personable and
readily admits to having many sexual partners in the past mostly
casual one-night stands with whom he usually uses
condoms. However, at time of presentation, he has been with his
current girlfriend for over a year and they no longer use condoms.
The man reports that while his girlfriend was away last weekend,
he went to a nightclub and met a woman with whom he had sex.
He was very drunk and is unsure whether a condom was used. He
tested negative to an HIV antibody test two years ago in another
city. He denies any same-sex partners or injecting drug use.
The GP conducts a screening for sexually transmissible
infections, including urethral swabs, and suggests blood tests for
HIV, syphilis and HBV. The man seems a bit resistant to the idea at
rst, but then agrees. He accepts a script for ciprooxacin and
azithromycin and agrees to return in one week for his results.
The mans urethral swab grows Neisseria gonorrhoeae, as
expected, but his HIV antibody test is also positive. All other tests
are negative. The young man is shocked at the news. He admits
that he did not tell the full truth on his previous visit; in fact, most
of his casual partners have been male. He reports both insertive
and receptive anal sex without condoms and says he is most
likely to seek casual sex when he has been drinking heavily.
has transmitted HIV) with someone whose own
previous high-risk behaviour is unrecognised.
Many HIV-infected women fall into this category.
Making the diagnosis in these situations is depen-
dent on retaining an open mind about the possi-
bility of infection.
Sexual health context
A person diagnosed with a sexually transmissible
infection (STI) is likely to be at increased risk of HIV
infection. An STI can be a marker of recent or
past risk and genital inammation itself may have
put the individual at higher risk of HIV infection.
Full evaluation of a person with an STI includes
HIV, HBV and often HCV antibody testing.
Consideration of HIV risk should be made with
regard to all patients who present with an STI.
Although statistically the diagnosis of a heterosex-
ually acquired STI is unlikely to be accompanied by
HIV infection in Australia, the presence of an STI
calls at least for careful clinical assessment of the
actual risk with the informed cooperation of the
person. There is a medical and legal imperative to
investigate fully any patient diagnosed with an STI
or blood-borne viral infection (Chapter 13). Failure
to diagnose can lead to ongoing transmission as
well as clinical progression.
More than 20 years into the HIV epidemic,
there is some evidence that 100% use of condoms
is becoming less common among gay men in
Australia.
1
Surveys in Melbourne and Sydney
have shown increasing levels of reported unpro-
tected anal intercourse with casual partners, and
surveillance data reveal increasing rates of gonor-
rhoea in these populations.
2
Regular testing for
gonorrhoea and other STIs in men who have sex
with men who have casual sexual partners should
be a routine part of clinical care. All gay and
bisexual men should be assessed for HAV and
HBV immunity and vaccinated if necessary.
In addition to triggering consideration of HIV
and HBV infection, the presence of an STI pro-
vides the primary care clinician with the opportu-
nity to take a sexual history and promote safe sex
practices (Chapter 3).
Risk factors for transmission
Although HIV, HBV and HCV are all blood-
borne viruses, the efciency of transmission in dif-
ferent settings varies enormously (Table 2.1).
Transmission will depend on many factors,
including the infectivity of the source (e.g. the
CASE STUDY 3
Sexual health context: an STI indicates the need
for HIV testing
Sexually transmissible infections
A young, openly gay man in a regional city presents to a GP with a
four-day history of a very painful anus, which he assumes to be
haemorrhoids, as he has suffered them previously. He says he has
never had anal sex. On examination, there are extensive perianal
ulcers and the GP takes swabs for herpes, gonorrhoea and
chlamydia. The young man is appalled that he could have a
sexually transmissible infection (STI), and the GP encourages him
to talk about his sexual history. The patient states that he only
ever has safe sex and has never had an STI. He reports a negative
HIV antibody test about two years ago and he has been vaccinated
successfully against HBV. He averages about three different
sexual partners a month at the local beat and he has never
injected. Upon further questioning about his sexual behaviour, the
patient reports that he and his most recent partner had done just
about everything two guys can do, short of fucking. When
questioned, he agrees that there had been some oral-anal contact
both ways. The GP suggests pharyngeal and anal swabs and
raises the issue of HIV testing. The patient readily agrees. The anal
swab returns positive for Herpes Simplex Virus (HSV) type 1 but
cultures for gonorrhoea and the HIV antibody test are negative.
CASE STUDY 4
HCV prevalence and transmission: past injecting drug
use may have caused infection
Past injecting drug use
Angeli is a 29-year-old solicitor who is four-months pregnant.
Upon routine testing, her GP discovers that Angeli has slightly
raised liver function tests (ALT 68 IU). She is otherwise in perfect
health. She presents with her husband and reports no risk factors
for HBV or HCV infection and is unvaccinated for HBV. She
describes herself as healthy and clean-living. Upon
investigation, it is discovered that Angeli is anti-HBc-negative but
HCV antibody positive. When seen on her own, Angeli reports that
she injected amphetamines on one or two occasions at age 19
years while a university student. Although she does not recall
sharing injecting equipment, she admits that the memories are
very hazy as she had been drinking on those occasions and had
allowed a friend to inject her. She has told no one about this drug
use, not even her husband, whom she fears will not understand.
She is deeply upset that this brief experimentation has come back
to haunt her current life and health, and she has fears that it could
affect her husbands and babys health. She is much relieved to
hear that the risk of transmission to her baby is quite low and that
transmission to her partner very unlikely.
can reduce the risk of perinatal transmission of
HIV and HBV to less than 5%.
5,17
In contrast to the lower efficiency of HCV
transmission in the sexual contact setting, HCV is
probably more efciently transmitted than HIV or
HBV through blood-to-blood contact where inject-
ing equipment (including swabs, spoons, water,
tourniquets, needles and syringes) is shared.
6
The non-specific nature of symptoms and
signs of both HIV and chronic viral hepatitis prior
to advanced disease makes the assessment of risk
behaviour a crucial component of the initial diag-
nosis of these conditions.
Prevalence and transmission
The likelihood of transmission after a specific
exposure is also related to the risk of infection in
the source. Although transmission of blood-borne
viruses is associated with certain risk behaviours,
prevalence rates are higher in specic groups in
viral load of HIV, HBV or HCV) and the type of
exposure.
The clearest example of the differences in
transmissibility of these three viruses is sexual
contact. Unprotected anal or vaginal sex with a
positive person carries a high risk of transmission
for both HIV and HBV but a very low risk of
transmission for HCV (Table 2.1).
3
The explana-
tion for this disparity is the absence (or extremely
low concentration) of HCV found in semen or
vaginal secretions, in contrast to the high levels of
both HIV and HBV in these bodily uids.
4
There are also differences in perinatal trans-
missibility of HIV, HCV and HBV. HCV has a rel-
atively low efciency of transmission in the peri-
natal setting; only 5% of infants born to women
with HCV will become infected, with factors such
as maternal viral load and duration of labour
affecting risk of transmission. Without interven-
tion, mother-to-child transmission of HIV and
HBV is common. However, proven interventions
2 Might this patient be positive? Epidemiology and transmission
TABLE 2.1 Risk of HIV, HBV and HCV transmission (from a known positive source)
HIV HBV
1
HCV
2
Sexual contact
Unprotected anal (receptive) very high very high very low
3
Unprotected anal (insertive) high very high very low
3
Unprotected vaginal high
4
very high very low
3
Unprotected oral (cunnilingus and fellatio, receptive and insertive) very low low-moderate negligible
Mother to child (perinatal)
No intervention 20-45% 30-90% 5%
5
With intervention <5%
6
<5%
7
NA
8
Occupational exposure (needle-stick) 0.3% 20-40% 2-10%
Sharing injecting equipment among IDUs very high very high extremely high
9
Unsterile tattooing and piercing high very high very high
Unsterile medical and other procedures high high high
1 Refers to chronic hepatitis B (HBsAg+), with higher risk where source is HBeAg+ and/or HBV DNA+.
2 Refers to chronic hepatitis C (HCV RNA+).
3 Higher risk may be associated with certain practices or circumstances where there is the possibility of blood-to-blood contact
(e.g. traumatic sexual practices, sex during menstruation) or high HCV viral load (e.g. HIV coinfection).
4 Some evidence of higher risk for male-to-female than female-to-male transmission.
5 Higher risk (15-20%) in presence of HIV/HCV coinfection, related to higher HCV viral load.
6 Proven interventions include antiretroviral therapy, caesarean section and avoidance of breastfeeding.
7 Intervention includes HBV immunoglobulin and vaccination.
8 There is no currently proven intervention for perinatal HCV transmission.
9 Some evidence of HCV transmission when sharing injecting equipment other than needles (e.g. spoons, tourniquets).
Australia: HIV in men who have sex with men;
HBV and HCV among injecting drug users
(IDUs); HBV in indigenous Australians and
Asian-born populations; and all three viruses in
people with haemophilia (Table 2.2). The low
prevalence of HIV in people other than homosex-
ual men in Australia accounts for the relatively
low risk of HIV infection after unprotected
heterosexual exposure and sexual assault.
Prevalence of HCV is very high among per-
sons who have ever injected drugs, and use of
injecting equipment that has been contaminated
with HCV-infected blood carries a very high risk
of transmission. Consequently, infection is com-
mon after even a small number of exposures, such
as the occasional sharing of injecting equipment.
TABLE 2.2 Prevalence estimates for HIV, HBV and HCV in Australia
1
HIV HBV
2
HCV
Injecting drug users 1-2%
3
40-50%
4
50-60%
3
Sexual orientation
Homosexual/bisexual men 5-10%
5
40-50%
4
5-7%
6
Homosexual/bisexual women <1% 2-5%
6
2-5%
6
Heterosexual men <1% 1-2% 1-2%
Heterosexual women <1% 1-2% 1%
Ethnicity
Indigenous Australians <1%
7
20-30%
8
2-5%
9
Asian <1% 20-30%
8
2-5%
10
Other <1% 1-2% 1-2%
Health care workers
11
<1% 1-2% 1-2%
Recipients of blood products
12
People with clotting disorders
13
20-30% 50-60%
7
0-80%
Other 1% 1-2% 2-5%
1 Some of these estimates are based on limited data, and should be considered as guides to levels of infection rather than true
prevalence values.
2 Based on prevalence of anti-HBc, indicating previous exposure. Approximately 95% of people exposed to HBV as adolescents/
adults clear HBV infection (HBsAg- and anti-HBs+) and are immune to re-infection.
3 Based on data from the National Needle and Syringe Program survey.
2
4 Prevalence of chronic hepatitis B (HBsAg+) estimated to be 2-3%.
7,8
5 Based on self-reported HIV status among gay men at gay community fair days in Australian capitals.
1
6 Higher prevalence estimates than heterosexual groups due to higher prevalence of injecting drug use.
9,10
7 Despite higher rates of other STIs, HIV prevalence is similar among indigenous and non-indigenous Australians.
11
8 The majority of transmission occurs during the perinatal period or early childhood, therefore the estimate for chronic hepatitis B
(5-10%)
12
is higher than for other high-risk groups (2-3% for IDU, homosexual men).
9 Higher estimate due to increased prevalence of injecting drug use and incarceration.
13
10 Higher estimate due to probable increased exposure through non-sterile medical, dental and other skin penetration procedures in non-
Australian born Asians. Higher estimated prevalence in people born in other selected, high prevalence countries (e.g. Italy, Egypt).
11 Although cases of occupational transmission of blood-borne viruses have been reported, including ve cases of HIV,
14
prevalence
of HIV, HBV and HCV is estimated to be similar to the general population.
12 In Australia, screening for HBV was introduced in the early 1970s, HIV in 1985, and HCV in 1990.
13 Includes people with haemophilia A, haemophilia B, and von Willebrands disease. In general, prevalence rates increase with
severity of clotting disorder and age (due to introduction of screening).
15
TABLE 2.3 Factors associated with increased or decreased transmission of HIV, HBV, HCV
Increased transmission
HIV Any:
High viral load in index case
Sexual:
Sexually transmitted infections in either partner
Genital inammation (includes STIs and
noninfectious vaginal inammation)
Occupational:
Deep penetrating injury
Hollow-bore needle
Perinatal:
Vaginal delivery
Breast-feeding
HBV Any:
Unvaccinated status
HBeAg+ or HBV DNA+ in index
HCV Any:
HCV RNA+ index case
High HCV viral load in index case
Decreased transmission
Any:
Low viral load (possibly through therapy)
Post-exposure prophylaxis (antiretroviral therapy)
Sexual:
Condoms and safe sexual practices
Treatment of sexually transmitted infections
Occupational:
Universal (standard) precautions
Perinatal:
Antiretroviral therapy
Caesarean section
Bottle-feeding
Any:
Vaccination
Post-exposure prophylaxis (immunoglobulin and vaccination)
Any:
Negligible risk of transmission if source HCV RNA-negative.
Use of sterile, unused, injecting equipment in a safe
environment.
2 Might this patient be positive?
The global HIV epidemic and its
implications for Australia
Outside Australia, the patterns of HIV transmis-
sion are extraordinarily diverse. Many countries in
Europe and North America are seeing extensions
of the HIV epidemic into ethnic and social minori-
ties, immigrant groups and the socially disadvan-
taged. HIV infection levels in injecting drug users
are often very high. In much of sub-Saharan Africa,
HIV is extremely prevalent, reaching 3040% in
young adults in some countries. High rates of geni-
tal ulceration and poor access to medical services
and preventative education account, in part, for
high prevalence rates. In some communities in
Australia (particularly remote Aboriginal commu-
nities) and in some of our nearest neighbours
(including Papua New Guinea), the same combina-
tion of factors exists (poverty, marginalised popula-
tions, high rates of STIs) that have allowed such
explosive epidemics in other countries.
In Asia, four countries (Thailand, Myanmar,
Indonesia and Cambodia) have adult prevalence
rates of over 1% and within these countries there
are certain populations, particularly injecting
drug users and sex workers, with much higher
HIV prevalence.
CASE STUDY 5
HBV transmission: perinatally acquired infection
HBV prevalence and transmission
Aaron is an 18-year-old medical student who consults his GP for
hepatitis B vaccination. Pre-vaccination screening reveals that he
is anti-HBc+ and HBsAg+. Aaron was born in Australia and his
parents are university academics who arrived in Australia from
south-eastern China in the mid-1970s. He is not aware of any
hepatitis in the immediate family but his grandmother died of liver
problems at a very old age. Due to Aarons potential infectivity,
his GP advises him to discuss his HBV-positive status with his
girlfriend and housemates. He is also advised to discuss his HBV
status with his family, with a view to subsequent HBV testing. Due
to the possibility of perinatally acquired infection, his GP stresses
the particular importance of HBV testing for his mother.
Travellers to regions of high prevalence of
HBV or HIV should be informed of the risks of
acquiring these infections through sexual or acci-
dental exposure.
The global pattern of HIV infection is begin-
ning to be reected in the pattern of heterosexual
HIV transmission in Australia. Immigrants from
high prevalence countries and their partners fea-
ture prominently amongst those newly diagnosed,
as do visitors to high prevalence regions. During
19982002, over 50% of people who acquired
HIV through heterosexual contact were from a
high prevalence country or had reported hetero-
sexual contact with a person from a high preva-
lence country.
2
Proven prevention strategies
There are several proven means of reducing the
efciency of transmission of HIV, HBV, and HCV
(Table 2.3). The use of condoms for anal or vagi-
nal sex and the use of clean injecting equipment
remain the most effective means of prevention of
transmission of HIV (Chapter 3). Other interven-
tions such as post-exposure prophylaxis may also
have a role in prevention (Chapter 4). Antiretroviral
therapy, caesarean section, and avoidance of
breast-feeding have reduced the risk of perinatal
transmission of HIV to less than 5%.
16
HBV vaccination is safe and extremely effec-
tive. Nevertheless, many people at risk of infec-
tion remain unvaccinated in Australia. The search
is currently underway for effective HIV and HCV
vaccines, but these may be a decade away.
Summary
HIV, HBV and HCV are different and distinct
viral infections in terms of epidemiology and risk
factors for transmission, although some points of
similarity occur, particularly in regard to modes of
transmission. The recommendation to test for
HIV, HBV and HCV should be based on reported
risk factors for transmission or clinical signs. A
low threshold for testing is advised due to the
reluctance of some people to disclose risk behav-
iours or their failure to identify risks.
References
1 Prestage G, Van de Ven P, Knox S, Grulich A,
Kippax S, Crawford J. The Sydney Gay Community
Periodic Surveys 1996 1999: Changes over time.
Sydney: National Centre in HIV Social Research
(NCHSR); 1999.
Research (NCHECR). HIV/AIDS, viral hepatitis and
sexually transmissible infections in Australia. Australian
HIV Surveillance Report. Sydney; NCHECR; 2003.
(available at Internet address
www.med.unsw.edu.au/nchecr)
3 Royce RA, Sena A, Cates W, Cohen MS. Sexual
transmission of HIV [published erratum appears in
New Engl J Med 1997;337:799]. New Engl J Med
1997;336;1072-1078.
4 Dore GJ, Kaldor JM. Detection of HCV RNA in
semen (letter). Lancet 2000;356:1520.
5 Dore GJ, Kaldor JM, McCaughan GW, et al.
Systematic review of role of polymerase chain
reaction in dening infectiousness among people
infected with hepatitis C virus. BMJ 1997;315:333-
337.
6 MacDonald M, Crofts N, Kaldor J, et al.
Transmission of hepatitis C virus: rates, routes, and
cofactors. Epidemiol Rev 1996;18(2):137-148.
7 Anderson B, Bodsworth NJ, Rohrsheim RA,
Donovan BJ. Hepatitis B virus infection and
vaccination status of high risk people in Sydney:
1982 and 1991. Med J Aust 1994;161(6):368-371.
8 Crofts N, Hopper JL, Milner R, Breschkin AM,
Bowden DS, Locarnini SA. Blood-borne virus
infections among Australian injecting drug users:
Implications for spread of HIV. Eur J Epidemiol
1994;10(6):687-694.
9 Bodsworth NJ, Cunningham P, Kaldor J, Donovan
B. Hepatitis C virus infection in a large cohort of
homosexually active men: independent associations
with HIV-1 infection and injecting drug use but not
sexual behaviour. Genitourin Med 1996;72:118-122.
10 Fethers K, Marks C, Mindel A, Estcourt CS. Sexually
transmitted infections and risk behaviours in women
who have sex with women. Sex Transm Inf
2000;76:345-349.
11 Guthrie JA, Dore GJ, McDonald AM, Kaldor JM, for
the National HIV Surveillance Committee. HIV and
AIDS in Aboriginal and Torres Strait Islander
Australians. Med J Aust 2000;172:266-269.
12 Gust ID. Epidemiology of hepatitis B infection in the
Western Pacic and South East Asia. Gut
1996;38(Suppl. 2):S18-S23.
13 Correll P, MacDonald M, Dore G. Hepatitis C
infection in indigenous communities in Australia.
Hepatitis C: informing Australias national response.
Canberra: Department of Health and Aged Care;
2000:47-60.
Research (NCHECR). Australian HIV Surveillance
Report 11(3). Sydney: NCHECR; 1995.
15 Leslie DE, Rann S, Nicholson S, Fairley CK, Gust ID.
Prevalence of hepatitis C antibodies in patients with
clotting disorders in Victoria: relationship with other
blood borne viruses and liver disease. Med J Aust
1992;156:789-792.
16 Gibb DM, Tess BH. Interventions to reduce mother
to child transmission of HIV infection: new
developments and current controversies. AIDS
1999;13(sA):S93-S102.
17 Mandelbrot L, Landreau-Mascaro A, Rekacewicz, et al.
Lamivudine-zidovudine combination for prevention
of maternal-infant transmission of HIV-1. JAMA
2001;285:2083-2093.
Introduction
Rapport, trust and effective communication are
vital components of the doctor-patient relation-
ship and contribute signicantly to a clinicians
ability to take a comprehensive history, particu-
larly in the context of the sensitive issues around
HIV and viral hepatitis. A thorough sexual and
drug-use history is required to identify specic
risk factors and behaviours of concern regarding
HIV and viral hepatitis, to establish a diagnosis
and to provide a setting for targeted prevention
and harm reduction messages and strategies.
Effective communication skills permit and
encourage patient involvement in decision-mak-
ing processes. This participation is associated
with greater patient satisfaction, increased com-
pliance with treatment and the creation of a rela-
tionship in which the patient feels comfortable
raising issues such as death, grief and relationship
or sexual problems.
1,2
3
Talking with the patient:
risk assessment and history-taking
Sarah Huffam Infectious Diseases Physician, AIDS/STD Unit and Royal Darwin Hospital,
Northern Territory.
Paul Haber Head of Drug Health Services, Royal Prince Alfred Hospital, Camperdown, New South Wales.
Jack Wallace Executive Ofcer, Australian Hepatitis Council, Canberra, Australian Capital Territory.
Key points
Sexual and/or drug history-taking begins with general issues
and progresses to more detailed and specic questioning
regarding risk behaviours.
Factors that will assist effective communication during sexual
and drug history-taking include:
a comfortable space and adequate time;
privacy and the absence of interruptions;
assurance and explanation of condentiality;
a non-judgemental attitude;
a willingness to discuss sexual and drug-use behaviour
in detail;
careful listening to the patient;
a focus on the goals of the interview.
The cultural appropriateness of sexual history-taking may
require consideration, particularly with regard to the gender of
the clinician.
General issues
Taking a sexual and drug-use history helps to
ascertain the patients risk of blood-borne diseases
and sexually transmissible infections (STIs). To be
effective, the process needs to be thorough and
several factors should be considered before start-
ing the interview.
The physical environment needs to be conducive
to private discussion and adequate time must be set
aside. If one appointment is not sufcient, allow for
further discussion when the patient returns for
his/her test results or follow-up, or suggest that
the patient return another day to complete the
interview.
Key elements of effective communication are
listening carefully and being interested, non-
judgemental and observant. Taking notice of the
patients unspoken cues and reecting back the
most salient points may assist communication.
Reection is a very simple technique that gives the
patient the opportunity to correct any misunder-
standings and allows the clinician to check that
he/she is on the right track.
One approach is to introduce the topic and
explain to the patient the reasons for such detailed
and private questioning. An opening statement
that normalises the discussion may be useful. For
example: Do you have any concerns about your
risk of exposure to hepatitis C, HIV or other sex-
ually transmitted infections? The clinician may
then state that it is important to raise these issues
with all patients. Initial, open-ended questions
should be followed by more detailed questioning.
The clinician may begin by addressing the least
confronting issues, followed by specic questions
when the patient appears comfortable.
Communication style and language will vary
depending on the clinician and the patient. The
clinician is advised to use language with which
he/she feels comfortable and familiar, and that
takes account of the language used by individual
patients. If the clinician doesnt understand a
word or phrase the patient has used, an explana-
tion should be requested. This helps to develop
trust and a sense of engagement, as well as clarity
of information.
The clinician should assure clients that conden-
tiality will apply to all information obtained in the
context of clinical service delivery. Condentiality
issues may be especially important for adolescents
and those living in smaller communities. While
reassuring the patient, make clear early on that
there are limitations to condentiality in every
jurisdiction, such as the requirement to report
individuals who deliberately and repeatedly put
others at risk of HIV infection or to notify author-
ities where there is evidence of child abuse.
A major barrier to effective communication is
awkwardness and embarrassment of patient and
clinician when discussing sexual practices or recre-
ational/injecting drug use. In particular, a clinician
who has a long-standing relationship with a
patient may be unable to broach certain topics.
Alternatively, he/she may have difculty raising
sexual matters with patients of the opposite gender
or of a different sexual orientation or age group.
Lack of training, time constraints and limited
knowledge of cultural and lifestyle issues can result
in a reluctance by the clinician to persevere with
these interviews.
3,4
A simple lack of practice also
may impede a clinician in taking a sexual and drug-
use history. For issues that challenge the values or
beliefs of the clinician, discussion with a colleague
may help to familiarise him/her with unusual or
challenging language or concepts.
Although patients are often reluctant to report
stigmatised behaviour, they may feel unable to
discuss their behaviour with friends or family. If
they feel they can trust the doctor, they may be
happy to talk about their risk behaviours in the
clinical setting. However, the clinician may need
to initiate this discussion.
It is useful to consider strategies for managing
conversations that become awkward or difcult
(Table 3.1). Breakdown in communication is very
common and may result in a change of topic. If
the interview is progressing poorly, it may be help-
ful for the clinician to consider his/her own
responses to the content of the discussion. It is
vital to be aware of the cues the patient is giving
and to try to ensure his/her needs are met by the
consultation. Empathy, humour and digression
may help to dissipate anxiety. Clarifying or redi-
recting statements, such as Could I ask another
question about HIV? can help to structure the
interview.
Despite knowledge and experience, interviews
dont always go well and referral to another clini-
cian or service may be appropriate.
Risk assessment
General medical history
It is less threatening to discuss general medical
history rst and then lead into a more specic
sexual and drug-use history. Early in the inter-
view, non-threatening questions relating to HIV,
HBV and HCV may be asked. These questions
may address:
a history of blood transfusions;
tattoos (including where, when and whether
done professionally);
country of birth and residence;
cultural practices (such as initiation ceremonies);
family history;
vaccination history;
piercing.
Drug-use history
Table 3.2 provides a checklist of information to
gather when taking a drug-use history. General
questioning may address the use of prescription
medications, tobacco and alcohol, followed by
use of non-prescription and illicit drugs. High
levels of alcohol consumption can play a signi-
cant role in sexual risk-taking and may be a target
for discussion about risk reduction. Non-prescrip-
tion drugs may also alter judgement and be a fac-
tor in the assessment of sexual risk. In addition,
the sharing of straws or other equipment used to
snort drugs has some risk of HCV transmission.
TABLE 3.1 What prevents effective communication?
Poor physical environment (lack of privacy, lack of time, interruptions)
Uncertainty about condentiality
Insufcient language skills or lack of a satisfactory interpreter
Inability to persevere through awkward times in the interview
Assumptions about sexuality and behaviour
A judgemental attitude (displaying lack of interest or prejudice)
Not listening to the patient
Inappropriate use of open and closed questions
Interrupting the patient excessively
Injecting drug use history
Important information to obtain about injecting
drug use includes:
whether and when any needles or injecting
equipment were shared;
the types of drugs injected;
the frequency of drug use;
the duration of drug use;
the most recent occasion of use.
Interviews about drug use should be informed by
a basic knowledge of common injecting drug use
equipment and practice, and the potential for
HCV transmission at all stages of the injecting
process. Table 3.3 contains a summary of drug
use language and equipment and Table 3.5 has a
summary of safer injecting practices. Chapter 14
provides details of some relevant referral and
information services.
Gathering detailed information will assist the
clinician to assess the patients risk of acquiring
and transmitting infections, as well as the possible
duration of infection. Drugs that may be injected
include performance-enhancing substances such
as steroids, as well as amphetamines, ecstasy,
benzodiazepines and opiates such as heroin.
Frequency and duration of use vary considerably;
risk behaviour may consist of a few episodes of
sharing injecting equipment many years ago,
which the patient may be reluctant to disclose. It
may be useful to suggest: Many people have
indicated that they have injected only one or two
times many years ago could this be the case with
yourself?
1
Other useful questions regarding drug
history are outlined in Table 3.4.
Health promotion about harm or risk
reduction with regard to injecting drug use
requires the clinician to have knowledge of safe
procedures and information about local services,
such as needle and syringe programs (Table 3.5
and Chapter 14). It is appropriate to discuss
whether the patient wishes to reduce or cease drug
use, and whether he/she would like referral to an
appropriate treatment service. Alternatively, non-
injecting routes of administration, such as
snorting and swallowing, may reduce risk.
Sexual history
The purpose of taking a sexual history is to assess
and limit the risk of acquisition of infection with
HIV or another STI. Sexual orientation or identity
does not always equate with particular behaviour,
therefore information about sexual practices, barri-
er/ condom use and the risk behaviours of sexual
TABLE 3.2 Drug history checklist
Drug use (past and present)
Type of drugs used (prescription, alcohol and tobacco, illegal)
Routes of administration
Sharing of injecting equipment (including swabs, lters, water, etc.)
Associated harms and evidence of dependence
Motivation to cease drug use or use non-injecting routes of
administration
TABLE 3.4 Useful questions about injecting drug use
Have you ever injected?
What do you inject?
How often do you inject?
Do you inject alone, or with other people?
Have you shared needles or other injecting equipment?
Do you know how to inject safely?
Have you ever overdosed?
Do you binge on drugs at certain times?
Do you know how hepatitis C is transmitted?
Are you concerned about your drug use?
TABLE 3.3 Injecting drug use equipment and language
Common injecting equipment
The drug(s); water; spoon; lter; swab; tourniquet; syringes;
needles; disposal containers.
Language
The mix (drug and water); mixing; jacking back (obtaining a blood
ashback in the syringe); pick (needle or needle and syringe); t
(needle and syringe); whack (either needle and syringe or the
drug); whacked or hit (an injection of drugs); user (person who
injects drugs); works (equipment); Harry (heroin); the gear (illicit
drugs generally); goey, whiz or speed (amphetamines).
3 Talking with the patient: risk assessment and history-taking
partners is more specific and useful than the
patients stated sexual orientation and/or marital/
partnership status. Common and often incorrect
assumptions are related to heterosexuality,
monogamy and preferred sexual practice.
The clinician should ascertain whether vaginal
or anal penetration has taken place. Questions
about anal sex should be asked of both men and
women and, in the case of male-to-male sex, it
should be determined whether penetration was
receptive, insertive or both. Oral sex confers a
lower risk of HIV transmission and may take the
form of oro-penile (fellatio), oro-vulval (cunnilin-
gus) and oro-anal (rimming/anilingus) sex.
Penetration of the vagina or anus with sex toys,
ngers or hands is generally considered low risk.
However, this type of penetration may result in
trauma that can provide a portal of entry for
infection. The clinician may need to establish the
nature of non-penetrative practices. Some non-
penetrative practices such as mutual or non-
shared masturbation are low-risk activities. Other
non-penetrative sexual practices, such as sado-
masochism and piercing during sex (which may
involve mucosal trauma or blood-to-blood con-
tact), may have a moderate-to-high risk of trans-
mission. Examples of questions to be asked dur-
ing sexual risk assessment are listed in Table 3.7.
When asking about sexual practices it is
important that the clinician and patient under-
stand each other. The clinician may seek to max-
imise understanding through specic questioning,
explanation and clarication. Have you been sex-
ually active? may be taken to mean only vaginal
or anal penetrative sex, so it may be appropriate
to indicate that the question also relates to oral or
other sexual activity. Specic questions such as
Do you ever have oral sex, where you suck on his
penis? Does he ejaculate (or come) when his penis
is in your mouth? or Does your partner ever
bleed following vaginal penetration? may be use-
ful in establishing the level of risk. Table 3.6 pro-
vides a checklist of information to gather when
taking a sexual history.
Where appropriate, condom use should be
explored in detail. Questions relating to condom
usage, as outlined in Table 3.7, form part of risk
assessment and provide an opportunity to discuss
effective safer sex practices. In addition, discus-
sion may address other safe sex measures. For
example, cervical diaphragms may offer some
protection and latex dams can be used for oral-
anal and oral-vaginal sex by men and women.
Latex gloves or condoms can be used for
TABLE 3.5 Safe injecting procedures
5
1 Preparation
Choose a safe place to inject. Avoid injecting alone.
Clean the area where you will be mixing.
Have everything you need within reach.
Wash hands (with soap and water or swabs).
2 Mixing up
Clean the spoon with a swab.
Put drugs into spoon.
Use a new sterile t to draw up water from new ampoule of
water (or cooled boiled water in a clean glass).
Do not put a used syringe into a group mix.
Add water to the spoon with the drugs mix.
Add lter to mix.
Draw solution up through lter to remove impurities.
Remove air bubbles.
3 Injecting
Wipe injection site with swab.
Place tourniquet around arm above injection site (dont leave it
on too long).
Put the needle into your arm at 45
o
angle.
Pull back the plunger; blood should appear in the needle. If no
blood remove needle, stop blood ow and try again.
When you are sure the needle is in a vein, loosen tourniquet
and depress the plunger, injecting solution.
Remove needle and apply pressure to site to stop blood ow.
4 Clean up
Rinse your t with cold water (reduces contamination risk and
gets rid of some blood in case t is to be used again
Appendix 4).
Dispose of rinsing water.
Dispose of t (recap your own, never recap another persons
syringe).
Wipe down the area where you have mixed up.
Wash hands and arms with soapy water (if not possible use
swabs).
Appendix 4 provides instructions on cleaning injecting equipment.
TABLE 3.6 Sexual history checklist
Number of sexual partners and their gender
Specic sexual practices
Presence of a sexual partner with an STI or with risk factors
for infection
Awareness of risk reduction techniques and extent of
compliance with these
Past STIs and their treatment
all the time. Occasions of risk-taking can be iden-
tied and explored. It is important that the patient
feels he/she can discuss episodes of unsafe behav-
iour without being judged or lectured. Gaining an
understanding of the patients perspective and
responding to his/her emotions will help in facili-
tating behavioural change. Common themes in a
discussion of risk-taking may include negotiating
safer sex with partners, drug and alcohol con-
sumption, or apathy and depression.
The clinician may engage the patient in gener-
ating his/her own solutions to unsafe practices.
Questions such as Has this happened before?,
What did you think or do on that occasion?,
TABLE 3.7 Risk assessment useful questions
Sexual practice
Do you consider that you might be at risk of HIV or
another sexually transmitted infection? (Detail what
activities may put someone at risk if necessary.)
Do you have any concerns about HIV or other STIs
(e.g. chlamydia, herpes)?
Are you sexually active?
How many sexual partners have you had? Over the
last three months? Since the last STI screen?
When did you last have a sexual partner?
Have you had any other sexual partners?
Are your sexual partners male, female or both?
What types of sexual activity do you engage in with
your partner? Vaginal? Oral? Anal? (Clarication may
be needed.)
Have you ever had an STI (e.g. chlamydia, herpes,
gonorrhoea)?
Do you know whether your sexual partners have been
at risk for HIV or STI? Have your male partner/s had
sex with other men? Have your sexual partner/s ever
injected drugs? Have your sexual partner/s lived in an
area where many people have HIV?
Condom usage
Do you or your partner/s use condoms? Always or
how often?
When did you start using them?
When dont you use them?
What are your reasons for not using condoms?
Do you have any problems using condoms?
Do they t well?
Do you use a water-based lubricant?
Have any condoms broken?
When do you put the condom on? When the penis is
erect?
Other transmission risks
Did you have a blood transfusion or use blood products
before 1990 in Australia?
Have you had a medical procedure or blood
transfusion overseas? Where and when?
Do you have tattoos? (Ask for details.) Professionally
done?
Have you ever had a sexual partner or household
member who had hepatitis C or B?
Have you ever had a sexual partner or household
member who was at risk of hepatitis C or B?
Have you ever been in prison?
3 Talking with the patient: risk assessment and history-taking
digital/sex toy penetration. Lubricants may
reduce the risk of vaginal trauma and subsequent
infection.
Prevention and harm reduction
messages
Opportunities for harm reduction and safe sex
education often arise during assessment of risk.
The primary care clinician may take these oppor-
tunities to ensure the patient understands the risks
of sexual activity and drug use, as well as safe
practices. Many individuals will be well informed
about safer practices but may not adhere to these
What were the outcomes? and How did you
feel? may assist the patient to identify and avoid
particular situations and reinforce safe practices.
Acknowledgement of the difculties a person may
face in trying to adopt or negotiate safe sex or safe
injecting may facilitate a more productive discus-
sion. Consideration should be given to the dif-
culty in challenging entrenched cultural norms
such as boys are in charge of condoms or he
looked young and healthy, so he couldnt have
HIV.
If a clinician chooses not to explore safe sex
and harm-reduction strategies with a patient dur-
ing a consultation, this may be noted and raised
during a subsequent appointment. Alternatively,
the clinician may decide to refer the patient to
another service or clinician, a community group
or a specialist counsellor/educator (Chapter 14).
Table 3.8 provides a check-list of general tips on
safe sex and harm reduction education.
Cross-cultural issues
There is great potential for misunderstanding and
communication breakdown when talking to
patients about sexual practice and drug use in a
culturally and linguistically diverse country such
as Australia. Use of interpreters may help commu-
nication. For clinicians who work with a
signicant number of patients from a particular
ethnic or cultural group, it can be useful to learn
about relevant attitudes and practices prevalent in
that cultural group. Alternatively, the clinician can
ask the patient whether the line of questioning is
appropriate. In situations where it is difcult to
consult with a patient of the opposite sex,
arrangements should be made for the patient to
see another clinician if possible.
Patients with disabilities or
psychiatric problems
People of all ages and abilities may be sexually
active. Some individuals, such as people with
intellectual or physical disabilities, may have
particular problems accessing information and
harm reduction and safe sex measures, such as
condoms. They may also have particular
difficulty negotiating safer sex. Ensuring ade-
quate knowledge and support for people with
disabilities or psychiatric problems may require
involvement with family and carers, and con-
sideration of issues specic to the patients par-
ticular situation.
TABLE 3.8 Tips on safe sex and harm reduction messages
Check the patients understanding about sexual and drug-use
behaviours that carry risk of transmission.
Explore safe sex and safe using options (such as non-injecting
techniques) specic to the patients needs.
Discuss correct use of condoms and where they can be obtained.
Discuss where new ts can be obtained and the correct method
of cleaning ts (Appendix 4).
Discuss circumstances in which unsafe practice has taken place
or is likely to occur.
Discuss the link between alcohol and other drug use and
unsafe sex.
Summary
Detailed drug-use and sexual history-taking may
be conducted over several consultations and pro-
vides the basis for an accurate assessment of risk
for HIV, HBV and HCV infection, as well as other
infections. Clear and non-judgemental communi-
cation facilitates accurate history-taking and
appropriate management. Impediments to history-
taking may be overcome by application of good
communication techniques, consideration of the
patients particular needs and consultation with
colleagues. However, if impediments persist, refer-
ral to another clinician or service is recommended.
References
1 Curtis JR, Patrick DL, Caldwell E, Greenlee H,
Collier AC. The quality of patient-doctor
communication about end-of-life care: a study of
patients with advanced AIDS and their primary care
clinicians. AIDS 1999;13:1123-31.
2 Roberts KJ and Volberding P. Adherence
communication: a qualitative analysis of physician-
patient dialogue. AIDS 1999;13:1771-78.
3 Epstein RM, Morse DS, Frankel RM, Frarey L,
Anderson K, Beckman HB. Awkward moments in
patient-physician communication about HIV risk.
Ann of Intern Med 1998;128:435-42.
4 Epstein RN, Frafey BA, Beckman HB. Talking about
AIDS. AIDS Patient Care and STDs 1999;13:545-53.
5 Australian Intravenous Injecting League. Cleaning
Fits. Canberra: National Hepatitis C Education and
Prevention Program, Australian National Council on
HIV/AIDS and Related Diseases; 2001. Australian
Intravenous Injecting League. Safer Injecting.
Canberra: National Hepatitis C Education and
Prevention Program, Australian National Council on
HIV/AIDS and Related Diseases; 2001.
HIV diagnosis by clinicians and provides patients
with timely options for intervention choices, as
well as opportunities for receiving appropriate
referral and support.
Pathogenesis of acute HIV infection
Knowledge of the pathogenesis of primary HIV
infection in adults helps the clinician to understand
HIV-related pathology testing. Within 1224
hours of exposure, cells at the site of a mucosal
infection are infected with HIV. Forty-eight hours
after exposure, HIV has spread to regional lymph
nodes where rapid replication occurs within
immune cells, primarily CD4 cells. Cells in the gut,
central nervous system and skin cells also become
infected. Over the next 540 days, the host
immune response to massive HIV viraemia results
in the production of neutralising antibodies and a
cytotoxic T-cell response mounted by CD8 T-cell
lymphocytes. The T-helper CD4 cells control the
cytotoxic response but also are infected by HIV.
Many but not all of these infected CD4 cells are
killed by the cytotoxic CD8 responses, causing a
fall in the CD4 cell numbers. These changes can be
observed clinically by monitoring CD4 and CD8
cell counts in the peripheral blood.
The u-like symptoms of primary HIV infection
are caused by the release of cytokines during the
process of infection and immune response. As a
result of the immune response, the blood concentra-
tion of the virus (the viral load) falls and new CD4
cells are produced by the bone marrow via the thy-
mus. For reasons that are unclear, the cytotoxic
CD8 cell response is not able to clear or completely
control HIV, as occurs with other viral infections.
4
Exposure and acute HIV infection
Jonathan Anderson General Practitioner, Carlton Clinic, Victoria.
John McAllister Clinical Nurse Consultant, HIV and Communicable Diseases, St. Vincents Hospital,
Darlinghurst, New South Wales.
Jon Willis Research Fellow, Australian Research Centre in Sex, Health and Society, Melbourne, Victoria.
Philip Keen HIV/AIDS Educator, Australian Federation of AIDS Organisations,
Surry Hills, New South Wales.
Ronald McCoy General Practitioner, St Kilda, Victoria.
Andrew Grulich Epidemiologist and Public Health Physician, National Centre in HIV Epidemiology and Clinical
Research, Darlinghurst, New South Wales
.
Introduction
Early diagnosis, monitoring and treatment of
patients with recently acquired HIV infection can
signicantly alter the long-term course of HIV dis-
ease. Knowledge of the clinical signs and symp-
toms of primary HIV infection, as well as the
serological and virological markers, enables early
Key points
Early diagnosis of HIV disease has signicant potential
benets. Monitoring and treatment can delay progression to
clinical disease, and the likelihood of ongoing transmission
may be reduced through implementation of safe sex and risk
reduction strategies.
Acute HIV infection may be difcult to distinguish from other
acute viral illnesses. Clinical features that should alert the
clinician to the possibility of acute HIV infection in the presence
of a mild-to-severe u-like illness include a glandular fever-
like illness, meningeal involvement, a recent sexually
transmissible infection and transient neurological symptoms.
Post-exposure prophylaxis (PEP) may reduce the risk of HIV
infection if offered within 72 hours of HIV exposure.
When a patient presents reporting a high-risk exposure to HIV,
rapid referral to an antiretroviral prescriber, sexual health centre
or hospital emergency department is necessary.
Symptoms of primary HIV infection can usually be managed in
the primary care setting by the general practitioner. Decisions
about antiretroviral therapy need to be made in conjunction
with an HIV-experienced clinician.
While newly diagnosed patients may require ongoing specialist
services from a range of providers, the general practitioner
remains an important source of initial and continued
information and support.
Signs and symptoms
Signs and symptoms of acute HIV infection can
present as early as three days or as late as ten
weeks following transmission. Most commonly
they occur at 1014 days. The onset of symptoms
often coincides with the appearance of HIV anti-
bodies although the patient may be HIV antibody
negative for up to three weeks after onset of
symptoms. The duration of the illness is most
commonly 414 days but may be longer.
1,2
Approximately 5090% of patients report signs
or symptoms suggestive of primary HIV infection
at the time of seroconversion.
3,4,5,6
Patients who
experience symptomatic primary HIV infection
appear to have more rapidly progressive HIV
disease than those who do not.
Detecting primary HIV infection
Primary HIV infection:
acute retroviral syndrome
Familiarity with the range of presentations associ-
ated with primary HIV infection (also called acute
retroviral infection or seroconversion illness)
enables the early diagnosis and management of
HIV infection. Clinical suspicion of acute HIV
infection should be followed by a thorough risk
assessment (Chapters 2 and 3). As the symptoms
and signs of acute HIV infection are similar to
those of many common infections, the presence of
HIV infection is more likely when a recent high-
risk exposure has been reported.
TABLE 4.1 Symptoms and signs of primary HIV infection
7
Symptoms of HIV seroconversion illness
Symptom Frequency
Generalised Fever >80%
Lethargy and general malaise >70%
Myalgia and arthralgia 50-70%
Lymphadenopathy 40-70%
Night sweats 50%
Gastrointestinal Pharyngitis 50-70%
Diarrhoea 30%
Oral ulcers 10-30%
Neurological Headache 40-70%
Aseptic meningitis 24%
Transient reversible neurological signs Rare
(neuropathies, Guillain-Barr)
Skin Rash 40-80%
Genital ulcers 5-15%
Initial laboratory Thrombocytopenia 45%
ndings
Leukopenia 40%
Raised liver enzymes 20%
Diseases caused Oral/oesophageal candidiasis Rare
by transient
Gut infections
immunosuppression
Pneumocystis carinii pneumonia (PCP)
The frequency of symptoms varies and severity
ranges from very mild to very severe (Table 4.1).
No single symptom distinguishes acute HIV infec-
tion from other acute viral illnesses. However,
there are some factors that should alert the clini-
cian to the possibility of acute HIV infection in
the presence of a u-like illness such as:
Epstein-Barr seronegative glandular fever-
like illness;
u-like symptoms outside usual season
(e.g. myalgia, arthralgia, headache, malaise);
fever for more than three days;
maculo-papular rash;
meningeal involvement;
transient neurological syndromes (e.g.
Guillain-Barr syndrome, neuropathies);
recent evidence of sexually transmissible
infections or genital ulcers;
recent high-risk exposure.
Recent risk exposure
Patients reporting recent risk exposure should be
thoroughly assessed and monitored for HIV infec-
tion. The possibility of HIV infection can be an
emotionally difficult time for the patient.
Provision of full pre-test counselling is required to
prepare the patient for the possibility of a positive
diagnosis and to provide him/her with the required
information about HIV infection (Chapter 8).
For high-risk HIV exposures that have occurred
within the last 72 hours, post-exposure prophy-
laxis (PEP) should be considered. Case study 2 and
the Box entitled PEP: is prevention of HIV infec-
tion possible after exposure? in this chapter
address assessment and referral for PEP.
Potential exposure to HIV often indicates a
risk of HBV and/or HCV infection. Consequently,
investigations for HBV and HCV should be con-
sidered in the context of acute HIV infection
(Chapter 5).
Investigations
When risk assessment and/or clinical presentation
indicate the possibility of acute HIV infection,
laboratory testing ensures correct diagnosis. HIV
antibody tests (HIV ELISA and Western Blot)
may be negative or equivocal up to three weeks
after the start of primary HIV illness (Table 4.2).
However, HIV viraemia appears in the blood in
the early days of the illness and may allow detec-
tion of virus particles or proteins (antigens) in the
absence of antibodies. If available, tests for viral
antigens or proviral HIV DNA may facilitate
early diagnosis of HIV infection during the win-
dow period.
It should be noted that the molecular tests cur-
rently available in Australia (listed in Table 4.2)
do not have the mandatory Therapeutic Goods
Authority (TGA) approval needed for their use in
the primary diagnosis of HIV infection.
4 Exposure and acute HIV infection
TABLE 4.2 Pathology tests for diagnosis of primary HIV infection
HIV antigen tests
P24 antigen P24 antigen may become positive within a few days of symptoms
and be absent after two weeks.
Qualitative PCR for HIV DNA may become positive within a few days of symptoms
HIV DNA and negative at one month.
Quantitative HIV RNA HIV RNA viral load may become positive within a few days.
viral load by RT PCR However, the quantitative viral load assay is generally not recommended
b-DNA to diagnose acute HIV infection due to a reported low false-positive
rate in the acute setting (usually indicated by low viral levels).
HIV antibody tests
HIV antibodies EIA may take up to three weeks to become positive after onset
(EIA or ELISA) of clinical signs and symptoms.
HIV antibodies Western Blot may take up to three weeks to become positive
(Western Blot) after onset of clinical signs and symptoms.
Note: Other tests may be indicated and should be performed in conjunction with specialist centres and laboratories.
Molecular tests should therefore be considered
conrmatory (of an indeterminate serology result)
when used in this setting.
Interpreting test results with regard to acute
HIV infection can be confusing and, if necessary,
clinicians are advised to seek guidance from their
pathology laboratory or the National Serology
Reference Laboratory (Chapter 14).
Management of acute HIV infection
and recent exposure
Acute HIV infection
People with primary HIV infection can usually
be managed in the community by their own GP,
with the support of either an HIV-experienced
GP and/or a hospital-based specialist. Most of
the physical symptoms are treatable with
simple analgesics and antiemetics. Hospital
admission may be required occasionally for rehy-
dration or management of rare manifestations
such as encephalitis or Guillain-Barr syndrome
(Table 4.3).
Very early treatment with antiretrovirals
a controversy
Treatment of HIV infection during the early
stages of chronic infection remains a controversial
and changing area of HIV medicine. Some HIV
clinicians treat primary HIV infection with com-
bination antiretroviral medications after one or
more of the confirmatory tests have returned
positive. The rationale for treatment during this
phase of HIV disease is to minimise immune
system damage, to lower the viral replication set
point (Chapter 1) and to minimise viral dissemi-
nation throughout the body. Others have argued
that the early immune response to HIV may
require the ongoing presence of HIV antigens and
that disturbing this response may be harmful. In
addition, short-term and long-term side-effects of
therapy can be considerable (Chapter 9).
While there are theoretical benets associated
with early treatment, there have been no ran-
domised, controlled trials examining the efcacy
of very early treatment in terms of time to
progression to AIDS or death. Clinicians inexperi-
enced in the management of HIV infection need
to contact an HIV-experienced GP or hospital
centre to discuss further management. If the
patient proceeds with treatment during primary
infection, HIV-inexperienced clinicians are
encouraged to maintain contact with their
patients as part of the treatment team, especially
as newly diagnosed and infected people require
considerable information and support from a
trusted and accessible source.
Contact tracing
Contact tracing of individuals who may have
been exposed to HIV prior to identication of pri-
mary infection should be undertaken. Discussion
with the patient regarding how to proceed with
contact tracing may be appropriate. The clinician
may ask the patient to consider recent blood-to-
blood or sexual contacts as well as recent blood
donations. Review of appropriate State or
Territory guidelines and/or discussion with public
health authorities may be considered.
Public health notication
Public health authorities must be notied when
HIV infection has been diagnosed. In most States
and Territories notication can be undertaken by
clinicians or pathology laboratories, although
there are differences in legislative and regulatory
requirements (Chapter 13).
TABLE 4.3 Management of primary HIV infection checklist
Referral to an HIV-experienced GP and/or a hospital-based clinician.
Support for the primary care clinician from an HIV-experienced GP and/or a hospital-based clinician.
Physical symptom relief such as analgesia for headache, myalgia and arthralgia, and
antiemetics for nausea.
Appropriate treatment for opportunistic infections.
Psychosocial support of the patient by the clinician and referral to an experienced mental health
professional as appropriate.
Early and frequent follow-up.
CASE STUDY 1
Diagnosing and managing
HIV seroconversion illness
Severe u or HIV seroconversion illness?
John is a 39-year-old engineer who presents to his
general practitioner, Dr Lewis, with a u-like illness in
April. He has been unwell for a week with muscle aches
and pains, fever, headache and retro-orbital pain,
particularly upon lateral gaze. He has spent the last four
days on the couch at home and has noticed that his
urine is very dark.
Dr Lewis considers a differential diagnosis of HIV
seroconversion illness and conducts a risk assessment.
I need to ask some sensitive questions. Nowadays we
need to ask people about risk behaviours for HIV when
they present with an unusual u-like illness. Have you
done anything in the past few weeks that might worry
you or might put you at risk for HIV? What I mean is, any
unprotected sex or sharing needles?
John relates that he recently started a relationship
with Sam and that they have been having sex without
condoms for four months. They intended to have HIV
tests but hadnt got around to it. While John was HIV-
negative when tested last November, he is unsure when
Sam was last tested. John has been vaccinated against
hepatitis A and B and reports never using needles.
Given his high-risk activity for HIV transmission, Dr
Lewis suggests HIV testing to John: While lots of other
common viruses cause symptoms like this, we should
consider testing for HIV infection. The rst illness that
some people get when they are infected with HIV can
look like u. Following pre-test counselling, John
consents to testing for HIV and HCV. Three days later,
the laboratory rings Dr Lewis about Johns test results.
Results
Standard (EIA) test for HIV antibodies negative
P24 antigen test positive
Qualitative HIV DNA polymerase tests positive
Western Blot test result not ready
Liver enzymes slightly elevated
Hepatitis C antibodies negative
Johns tests conrm a clinical diagnosis of HIV primary
infection. He is referred to a GP experienced in the
management of HIV infection after indicating that he
would prefer to see a community-based HIV clinician.
After lengthy discussion about treatment options, the
HIV-experienced clinician and John decide to go ahead
with antiretroviral treatment.
Dr Lewis continues regular follow-up with John to
address his ongoing medical and psychosocial needs
following the HIV diagnosis. In addition to assistance in
taking medications, John raises relationship and
sexuality issues. Dr Lewis refers him to the local AIDS
Council for support and offers written resources for HIV-
positive people.
CASE STUDY 2
PEP presentation and issues of safe sex
and disclosure
PEP, safe sex and disclosure
David is a middle-aged, married man who presents to his
general practitioner, Dr Betheras, for HIV post-exposure
prophylaxis (PEP) the morning after a condom break during
receptive anal sex in a sex-on-premises venue.
Dr Betheras immediately organises referral to a
general practitioner who can prescribe antiretroviral
therapy.
Before David leaves for his next appointment, Dr
Betheras advises him that he will need to institute condom
use when having sex with his wife and any other sexual
partners until he has his nal, week-24 test results. How
will I explain this to my wife? David asks. Dr Betheras
explores his concerns about the risk episode and the fear,
guilt and shame he is experiencing. She also discusses with
him the issues involved in talking about the episode with
his wife, if and when he decides to do so.
David returns to see Dr Betheras several days later
to discuss the issue of safe sex.
He decides that he must tell his wife but is reluctant
to do so immediately. In the meantime, he decides to
say that he has a urinary infection and needs to use
condoms for a while. Dr Betheras suggests that it might
be a good idea to see a counsellor about these issues.
David agrees and referral details are provided.
Dr Betheras also discusses the case with her medical
insurer and gets advice about the legal issues of duty of
care and condentiality regarding both David and his wife
(Chapter 13). She continues to monitor the situation in
conjunction with the general practitioner providing PEP.
Supporting newly diagnosed patients
The ongoing psychological adjustment of patients
to HIV infection can be affected by the nature of
early consultations with their doctor after diagno-
sis. In particular, having a long consultation when
the HIV diagnosis is given has been positively cor-
related with better long-term adjustment, as have
the quality of information given and the attitude
of the person giving the diagnosis.
8,9
Newly diagnosed patients have major issues to
face and adjustments to make during early con-
sultations. For example, patients may suddenly
confront their mortality or have concerns about
future income and relationships with partners,
family and friends.
10,11,12
Patients with children often have concerns
about how their children will deal with the diag-
nosis and whether they will be able to continue to
provide for the children materially and emo-
tionally.
13
For women of childbearing age, there
may be fears and concerns about how HIV affects
their future reproductive life.
14
Simple acceptance,
in the face of perceptions of social stigma and dis-
crimination, may be the most valuable support a
clinician can offer in early consultations. Patients
may also need help in deciding whether to dis-
close their HIV status and, if so, to whom.
15
Emotional support and acceptance can also assist
the person to make benecial alterations to his/her
lifestyle, such as changes to diet and exercise, reduced
drug and alcohol use and practising safe sex.
11
Post-exposure prophylaxis: Is prevention of HIV infection possible after exposure?
There is some evidence that a four-week course of
antiretroviral therapy, commenced as soon as possible
within 72 hours of exposure to HIV, can reduce the risk of
HIV infection.
16
Such therapy is called post-exposure
prophylaxis (PEP). Antiretroviral therapy for HIV infection
is listed under Section 100 of the Pharmaceutical
Benets Scheme and can only be prescribed by
approved clinicians.
Risk assessment
To respond appropriately to a possible HIV exposure
requires an assessment of the likelihood of HIV infection
in the source, the risk associated with the exposure and
the effectiveness of treatment options. As detailed in
Chapter 2, highest risk is dened as sexual exposure to
an HIV-infected individual via receptive intercourse
(without intact condom) or exposure to HIV-infected
blood via injecting equipment where percutaneous
exposure has occurred with a used hollow needle.
For percutaneous, occupational exposures, the NSW
Needlestick Injury Hotline (1800 804 823) can provide
advice to health care workers regarding the level of risk
(Chapters 12 and 14).
Assessment should address whether the source is
known to have HIV infection and/or viral hepatitis or risk
factors for blood-borne viruses, including a history of
unprotected sex with homosexual or bisexual men, a
history of injecting drug use, or haemophilia (Chapters 2
and 3). If the source is available and willing, testing for
HIV and viral hepatitis should be conducted with full pre-
test and post-test counselling.
PEP
Following assessment, all individuals with high-risk
exposures should be immediately referred to an
approved antiretroviral prescriber, a sexual health centre,
or the emergency department of a major hospital for
provision of PEP. The sooner the post-exposure
antiretroviral treatment is commenced, the greater the
theoretical chance of success. Details of how to contact
antiretroviral prescribers are given in Chapter 14 and the
ASHM Directory.
PEP involves a one-month course of dual or triple
drug therapy. It must be taken strictly as prescribed to
reduce the risk of drug resistance. Antiretroviral drugs
cause common side-effects such as nausea and
diarrhoea as well as rare, severe side-effects, so
monitoring by an HIV clinician is required.
The possibility of exposure to HIV causes anxiety and
concern. Patients need considerable support at this time,
due not only to the possibility of new HIV infection, but also
to help manage the adverse effects of the antiretroviral
medications. Enabling a patient to examine and modify
his/her sexual and/or injecting drug use risk behaviours is a
vital component of the PEP process. Patients may require
referral to an experienced counsellor.
Testing for HIV antibody is required six months after
exposure to exclude the possibility of late
seroconversion. During this time, patients should adopt
safe sexual practices with all partners and should not
donate blood, body tissues or semen, and female
patients should not breast-feed infants.
National guidelines on the use of PEP for non-
occupational HIV exposures have been produced by
ASHM and endorsed by the Australian National Council
on AIDS, Hepatitis C and Related Diseases (ANCAHRD)
and the Inter-governmental Committee on AIDS, HIV and
Related Diseases (IGCAHRD). The guidelines are
available at http://www.ancahrd.org/pubs/index.htm or
by calling toll free (within Australia): 1800 022 863
Support services and the role
of the clinician
In addition to the support that clinicians can offer,
patients should be referred to other agencies for
information, counselling and support as appropri-
ate (Chapter 14). Research has identified the
importance of contact with HIV-positive commu-
nities in helping newly diagnosed patients come to
terms with their new status and continue with
their lives.
12
However, whilst acknowledging that specialist
counselling may best meet the psychosocial needs
of patients, clinicians must recognise that they
may be the rst and most important source of this
support and information in their patients lives.
This is especially true during the early stages of
HIV infection. Maintaining contact with the
patient after the initial diagnosis, as either the key
HIV-treating clinician or as a partner in care,
helps to support the patient through the many dif-
culties that may lie ahead.
Summary
The primary care clinician has a key role in identi-
fying cases of primary HIV infection and facilitat-
ing the clinical monitoring and management of
infected individuals. Following diagnosis of pri-
mary HIV infection, referral to an HIV-experi-
enced clinician is recommended for consideration
of antiretroviral therapy. To reduce the risk of
infection after a high-risk exposure to HIV, post-
exposure prophylaxis may be taken within 72
hours of the exposure. Reported exposure pro-
vides an opportunity to review risk behaviours,
safe sex practices and harm minimisation strate-
gies. Provision of information and psychosocial
support are key elements of management follow-
ing a possible HIV exposure or diagnosis with pri-
mary HIV infection.
References
1 Cooper DA, Maclean P, Finlayson R, et al. Acute
AIDS retrovirus infection: Denition of a clinical
illness associated with seroconversion. Lancet
1985;1:537-540.
2 Schacker T, Collier AC, Hughes J, et al. Clinical and
epidemiologic features of primary HIV infection. Ann
Intern Med 1996;125:257-264.
3 Tindall B, Barker S, Donovan B, et al.
Characterization of the acute clinical illness
associated with human immunodeciency virus
infection. Arch Intern Med 1988;148:945-949.
4 Keet IPM, Krijnen P, Koot M, et al. Predictors of
rapid progression to AIDS in HIV-1 seroconverters.
AIDS 1993;7:51-57.
5 Schacker T, Collier AC, Hughes J, et al: Clinical and
epidemiologic features of primary HIV infection. Ann
Intern Med 1996;125:257-264.
6 Lange JMA, Parry JV, de Wolf F, et al. Diagnostic
value of specic IgM antibodies in primary HIV
infection. AIDS 1988;2:31-35.
7 Adapted from Kahn JO, Walker BD. Acute HIV type
1 infection. New Engl J Med 1998:339;33-39 and
Vanhems P, Hughes J, Collier AC, et al. Comparison
of clinical features, CD4 and CD8 responses among
patients with acute HIV-1 infection from Geneva,
Seattle and Sydney. AIDS 2000:14;375-381.
8 Jackson LD and Selby MJ. Communicating an HIV-
positive diagnosis. In Roth NL and Fuller LK, (eds).
Women and AIDS: Negotiating safer practices, care,
and representation. New York: The Haworth Press;
1998:131-153.
9 Pergami A, et al. How should an AIDS diagnosis be
given? The view of patients. Int J STD AIDS
1994;5(1):21-24.
10 Rinken S. The event of diagnosis: Diagnosis of
HIV/AIDS as a crisis of self-description. Social
Systeme 1997;3(1):101-121.
11 Roth N and Nelson M. HIV diagnosis rituals and
identity narratives. AIDS Care 1997;9(2):161-79;
12 Kleine-Kraft AE. How HIV positive gay men perceive
seropositivity and what signicance they give this
diagnosis as evidenced by sexual behaviour
changes and care needs. Dissertation Abstracts
International: Section B: The Sciences and
Engineering. 1995;55(9-B):3817.
13 Thorne C, Newell ML, Peckham CS. Disclosure of
diagnosis and planning for the future in HIV-affected
families in Europe. Child Care Health Dev 2000;26(1):
29-40.
14 McDonald K, Grierson J, de Visser R and Bartos M.
A complex uncertainty: Women on health, hope and
living with HIV in Australia. Monograph Series
Number 19. Melbourne: Australian Research Centre
in Sex, Health and Society.
15 Mansergh G, Marks G, and Simoni JM. Self-
disclosure of HIV infection among men who vary in
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16 Lurie P, Miller S, Becht F, et al. Postexposure
prophylaxis after nonoccupational exposure. JAMA
1998;280:1769-1773.
naemia, or a syndrome of non-deforming arthri-
tis similar in distribution to rheumatoid arthritis.
Chronic HBV may also be associated with extra-
hepatic manifestations.
Symptoms and signs of acute hepatitis
The symptoms and signs of acute viral hepatitis
are not specic for a particular aetiological agent
and are the same for acute hepatitis and chronic
viral hepatitis (Chapter 7). They include: nausea,
vomiting, anorexia, lethargy, jaundice and tender
hepatomegaly. Patients who present with a pro-
longed prodromal illness, including arthralgia and
rash, may have immune complex disease associa-
ted with HBV infection. Rarely, acute liver failure
supervenes. Signs and symptoms of acute liver
failure include intractable vomiting, encephalopa-
thy, asterixis and fetor hepaticus.
5
Exposure and acute viral hepatitis
Jeffrey Post Infectious Diseases Physician, Infectious Diseases Department and Albion Street Centre,
Prince of Wales Hospital and Research Scholar, School of Pathology, University of New South
Wales, Randwick.
George Marinos Hepatologist, Viral Hepatitis Research Unit, Department of Gastroenterology, Prince of Wales
Hospital, Randwick, New South Wales.
Ingrid van Beek Public Health Physician, Director, Kirketon Road Centre, Kings Cross, New South Wales.
Mary Burns Coordinator Hepatitis C Helpline, Carlton South, Victoria.
Acute hepatitis
Epidemiology
In Australia, 400500 cases of HAV infection and
400 cases of newly acquired HBV infection are
reported annually.
1
An estimated 16,000 new cases
of HCV infection occur annually but only 400700
cases of newly acquired HCV are reported because
most cases are subclinical and go unnoticed.
1,2
Acute hepatitis secondary to excessive alcohol
consumption is also common. Various forms of
chronic liver disease may present clinically as an
acute hepatitis. These include autoimmune
hepatitis and Wilsons disease, as well as chronic
HBV, which may present as a hepatitis are. Drug-
induced hepatitis also should be considered in all
cases of sudden liver enzyme elevation.
Outcomes of acute hepatitis
Less than 1% of all cases of viral hepatitis with
jaundice develop acute liver failure. Infection
with HAV causes acute hepatitis but is not asso-
ciated with the development of chronic infec-
tion. In contrast, infection with HCV and HBV
can result in acute and chronic infection (Table
5.1). Infants and children infected with HBV are
more likely to develop chronic HBV infection
than adults. Early studies of HCV infection have
suggested that a signicant proportion (85%) of
people acutely infected develop chronic
viraemia. However, more recent studies suggest
that rates of chronic infection may be as low as
55%.
3
Chronic hepatitis secondary to HCV and
HBV infection may progress to cirrhosis, liver
failure and hepatocellular carcinoma (HCC).
Some patients with chronic HCV infection may
develop glomerulonephritis, mixed cryoglobuli-
Key points
The hepatotropic viruses (HAV, HBV, HCV) cause most cases
of acute hepatitis, although other infectious agents and drugs
need to be considered. Acute HCV infection is probably under-
recognised.
Primary care clinicians should make a denitive diagnosis
where possible, and refer patients with unclear diagnoses or
rare, treatable conditions. Patients should be monitored for
acute liver failure and hospitalised if signs are detected.
Primary care clinicians play a critical role in the prevention of
viral hepatitis. Interventions such as education, vaccination,
contact-tracing, post-exposure prophylaxis and public health
notication are critical to the control of epidemics and
prevention of disease in individuals at high risk.
Preventative interventions should be offered to persons with clinical
acute hepatitis, those recognised to be in at-risk populations and
those who have been exposed to hepatotropic viruses.
Incubation periods
The average time from exposure to the develop-
ment of symptoms varies for the three major
hepatotropic viruses:
HAV 3 weeks (range 27 weeks);
HBV 10 weeks (range 426 weeks);
HCV 7 weeks (range 221 weeks).
Diagnostic approach
The diagnosis of acute hepatitis relies predomi-
nantly on serological testing, although other fea-
tures are important to consider.
History should include consideration of:
symptoms consistent with acute hepatitis;
a review of any symptoms that may suggest
an alternative diagnosis (e.g. infectious
mononucleosis);
epidemiological clues (Table 5.1 and Chapter 2);
a history of alcohol and drug use (including
illicit drugs, over-the-counter medications and
complementary therapies);
travel history;
vaccination history;
family history of liver disease.
An awareness of current epidemiological informa-
tion is useful (such as a current outbreak of HAV).
Examination should specifically include
evaluation for fever, icterus, rash, arthritis, tender
hepatomegaly, splenomegaly, injection sites, tattoos,
piercings and signs of hepatic encephalopathy
(asterixis, fetor hepaticus and altered mental state).
A general examination should be performed.
Non-serological investigations
Basic investigations should include liver enzymes,
full blood count and coagulation prole. Specic
results can assist in establishing the cause of acute
hepatitis. For example:
In viral hepatitis, the ALT is usually 10100
times the upper limit of normal with the
AST/ALT ratio less than one.
In alcoholic hepatitis, the ALT is generally 210
times the upper limit of normal with the
AST/ALT ratio greater than 1.5; bilirubin is usu-
ally elevated.
In drug-induced hepatitis, a mixed prole may
be seen with raised hepatic (AST and ALT) and
cholestatic (alkaline phosphatase and GGT)
markers.
Atypical lymphocytosis may suggest a viral
aetiology and thrombocytopenia may indicate
acute alcohol exposure or the presence of
chronic liver disease with portal hypertension.
The coagulation prole may reveal a pro-
longed prothrombin time or INR suggestive
of liver failure.
Serological investigations
All serological investigations should be under-
taken after appropriate pre-test counselling and
the results given in conjunction with post-test
TABLE 5.1 Outcomes of acute viral hepatitis
Hepatitis A virus
Approximately 0.1% of patients with HAV develop acute liver
failure. Less than 40% of patients with acute liver failure die or
receive a liver transplant.
Chronic hepatitis does not occur following HAV infection.
Lifelong immunity occurs after infection.
Hepatitis B virus
Less than 1% of clinical cases develop acute liver failure.
8090% of patients with acute liver failure die or receive a liver
transplant.
Less than 5% of adults with acute HBV infection develop
chronic hepatitis.
90% of infants infected at birth develop chronic hepatitis.
Those who go on to develop chronic infection are at risk of
cirrhosis, hepatocellular carcinoma and liver failure.
Those with chronic infection have persistent HBsAg and are
infectious to others.
Those who clear infection have lifelong immunity, maintain
anti-HBc, and may or may not preserve anti-HBs.
Hepatitis C virus
Acute liver failure is rare, but may occur in persons with HBV
coinfection.
Approximately 75% of adults with acute HCV infection develop
chronic HCV.
Those who go on to develop chronic infection are at risk of
cirrhosis, hepatocellular carcinoma and liver failure.
5% of infants born to HCV-infected women develop HCV
infection.
If infection resolves and the virus is cleared, the person is NOT
immune and can be re-infected. After resolution of infection,
antibodies persist for a variable amount of time (20 years in
some cases).
5 Exposure and acute viral hepatitis
counselling (Case Study 1 and Chapter 8). Specic
serological investigations are indicated in
Flowchart 5.1 and Table 5.5.
If the diagnosis is unclear, the initial serologi-
cal investigations may be repeated after 12
weeks. Serological investigation of Epstein-Barr
virus infection and investigation of less common
causes of hepatitis can be undertaken at this time.
If the diagnosis is still unclear, specialist referral is
indicated.
Key considerations when testing
for acute viral hepatitis
In the context of acute HAV infection, anti-HAV
IgM is invariably present. False negative results
are rare.
Acute HBV infection is best detected by test-
ing for HBsAg and anti-HBc IgM. Anti-HBc IgG
and anti-HBs appear later in the course of the ill-
ness. HBV DNA is generally not used as a diag-
nostic tool in acute HBV infection. In patients
with HBV infection, hepatitis D virus (HDV)
should also be considered, particularly in a
patient with chronic HBV who develops a new
episode of acute hepatitis or if the disease is
severe. Anti-HDV IgG and IgM testing is avail-
able at a limited number of laboratories.
In acute HCV infection, HCV antibody may
be present at the onset of hepatitis or may develop
in the following weeks. If it is not present, and
HCV is suspected on epidemiological grounds,
HCV RNA polymerase chain reaction (PCR)
should be performed to detect viraemia directly.
HCV antibodies are usually present within three
months of exposure.
Supportive therapy
Most cases of acute viral hepatitis do not require
hospitalisation.
Hospital assessment is recommended for
patients who exhibit signs of encephalopathy, as well
as for patients who are unable to maintain an ade-
quate uid intake and/or have prolongation of the
INR or a rising bilirubin (greater than 300 mmol/l).
Most drugs should be avoided during acute
hepatitis. Analgesics are generally not required
and aspirin, narcotics and sedatives should be
avoided. Small amounts of paracetemol may be
used for management of constitutional symp-
toms. Patients should be advised to avoid alcohol.
If the cause of hepatitis is unclear, a careful med-
ical review should be undertaken and potential
hepatotoxins should be ceased. Small meals may
be easier for the patient to tolerate.
CASE STUDY 1
Hepatitis B diagnosis: managing the anxious patient
Anxious patient with acute viral hepatitis
Peter is a 19-year-old man of European background who presents
to a general practice clinic. He has recently been told by another
service that he has hepatitis B after an episode of jaundice. Peter
has no idea whether he has acute or chronic infection and
believes that it is for life. He is distressed and expresses fear
about sharing food with his family, kissing and hugging. Peter
believes that he will never be able to have sex again because he
is contagious.
Peter is confused about the differences between acute and
chronic infection, and he has an exaggerated sense of how easily
HBV can be transmitted. Infected people are often extremely
fearful of infecting loved ones and need accurate information from
health professionals to enable them to continue in their usual
activities and maintain closeness with family and friends.
The clinician contacts the other service, establishes how the
diagnosis was made and uses the serology and other
investigations to determine that Peter has acute hepatitis B
infection. Peter is queried regarding symptoms such as
intractable vomiting, disturbed sleep and altered mental state,
and examined for physical signs including asterixis (hepatic ap)
and fetor hepaticus, to ensure that there is no evidence of liver
failure. Peter agrees to have further liver function tests and INR as
recommended by the clinician.
Although serology shows Peter is negative for HCV and HIV
antibodies as well as HAV IgM, the clinician assesses Peter for
risk factors for viral hepatitis and discusses the ways in which
other blood-borne viruses and sexually transmitted infections can
be prevented.
The clinician explains how HBV is transmitted and,
importantly, also discusses ways in which it is not transmitted
(Chapters 1 and 2). The clinician states that over 90% of adults
clear acute HBV infection (Table 5.1) but even if Peter does
develop ongoing or chronic infection, he can still kiss, hug, share
food and even have sex without transmitting HBV. The clinician
explains that an effective vaccine is available for his loved ones
(Post-exposure prophylaxis and Immunisation in this chapter),
although Peter will need to use condoms for sexual intercourse
until any sexual partners are effectively vaccinated.
The clinician tells Peter that he requires follow-up for at least
six months to ascertain clearance or persistence of HBV infection.
Peter is invited to return the following week to discuss his test
results and review other issues discussed during the consultation.
Because of the fear and uncertainty associated with viral
hepatitis, it is especially important that health professionals give
accurate information about transmission and prognosis at the
time of diagnosis, and explore the availability of treatment options
if chronic infection with HBV develops.
In the case of acute HBV, infection will resolve
spontaneously in the majority of adults and antivi-
ral therapy is not indicated. It should be noted that
patients with undiagnosed chronic HBV may
develop severe spontaneous flares of hepatitis
which appear clinically as an acute hepatitis. In this
situation, resolution may be enhanced with nucle-
oside analogue therapy (Chapters 1 and 10).
Clinical monitoring
Liver function tests should be performed once or
twice per week in addition to an assessment of
coagulation prole and clinical status.
Acute liver failure is the most serious compli-
cation of viral hepatitis, occurring in less than 1%
of HAV and HBV cases. It remains unclear
whether acute HCV can result in acute liver fail-
ure. In viral hepatitis, acute liver failure results
from massive, immune-mediated hepatocyte
necrosis. Risk factors for the development of
acute liver failure in viral hepatitis are not fully
understood but older age and concomitant liver
disease have been implicated. Death may occur
even when the liver has begun to regenerate.
Altered mental status (hepatic encephalopathy)
and coagulopathy in the setting of acute hepatitis
denes acute liver failure. Typically, non-specic
symptoms such as malaise, nausea, intractable
vomiting and sleep disturbance develop in the pre-
viously healthy person, followed by jaundice, the
rapid onset of altered mental status and coma.
Thus, the patient goes from being healthy to mori-
bund within 210 days. Supportive laboratory
ndings include high serum ALT, low blood glu-
cose levels and worsening coagulopathy.
The management of acute liver failure begins
with the recognition that patients with coagulopa-
thy or encephalopathy may die. Due to the poten-
tial for rapid deterioration in their clinical status
and the need for close monitoring, patients with
acute liver failure are best cared for in hospital.
Liver transplantation may be required in a small
proportion of cases.
Referral to a liver transplant unit is indicated
where:
the patient is in a remote hospital;
there is any evidence of encephalopathy;
there is worsening coagulopathy.
To determine whether chronic infection has been
established, the recommended follow-up time for
acute hepatitis is at least six months. Repeatedly
normal ALT results and a negative HCV RNA PCR
at six months indicate viral clearance. Table 5.5 and
Flowchart 5.1 provide details of HBV follow-up.
TABLE 5.2 Clues to diagnosis epidemiological
and exposure risks
Knowledge of current epidemiology, e.g. HAV cluster
Contact with a case of acute or chronic hepatitis
Travel to endemic area without vaccination or passive prophylaxis
HAV, HBV, yellow fever
Travel to endemic areas HAV, HBV, HEV, dengue fever,
leptospirosis, etc.
Unprotected penetrative sex HBV
Unprotected oro-anal sex HAV
Occupation, e.g. sewerage workers, childcare workers HAV
Occupation, e.g. health care workers HAV, HBV, HCV
Injecting drug use HAV, HBV, HCV
Alcohol consumption
Family history HBV, Wilsons disease, alpha1-antitrypsin deciency
Country of birth HAV, HBV
Tattoos and/or body piercings HBV, HCV
Blood transfusion and medical/dental procedures HBV, HCV
Needle-stick injury or other signicant occupational exposure
HBV, HCV
History of imprisonment HCV
Specic therapy
There is little role for specic agents in the manage-
ment of acute viral hepatitis. However, in prolonged
cholestasis after HAV infection, corticosteroids may
reduce serum bilirubin and relieve itch. The role of
interferon and nucleoside analogues in the treat-
ment of acute HCV and HBV is not established.
Although individual clinical trials have been unable
to demonstrate a benet of interferon therapy in
acute HCV, meta-analysis has shown a benet of
interferon in terms of normalisation of ALT and
clearance of viraemia. It is unclear whether a strat-
egy of treating only those patients who develop
chronic infection is any less effective than treatment
during the acute phase.
4
Interferon therapy is not
currently available under Section 100 of the
Pharmaceutical Benets Scheme for acute hepatitis
C and referral to a specialist for advice is recom-
mended for patients considering treatment.
FLOWCHART 5.1 Diagnostic and management algorithm for cases of acute hepatitis.
ACUTE HEPATITIS ALGORITHM
CASE OF ACUTE HEPATITIS
Test for anti-HAV IgM, anti-HBcIgM, HBsAg, anti-HCV and others as suggested by history.
Monitor for acute liver failure (if develops refer to hospital).
Assess index for need for other vaccinations, testing, prevention and education strategies.
Drug history.
Acute HAV.
Acute HBV (note: may be
are of chronic HBV).
Consider testing for
acute HDV.
Acute HCV
(if seroconversion
demonstrated), or possible
chronic HCV.
Consider HCV RNA PCR
if risk factors. Repeat
initial serology. Test for
EBV IgM and IgG.
Re-assess history,
symptoms and signs.
Other diagnostic tests.
Anti-HAV IgM positive.
Anti-HBc IgM +/-
HBsAg-positive.
Anti-HCV positive.
Negative serology for
acute HAV, HBV and HCV.
No
diagnosis.
Refer to
specialist.
1. Notication.
2. Contact-tracing and
normal immunoglobulin
+/- vaccination.
1. Notication.
2. Contact-tracing,
testing, HBIG and
vaccination as required.
Education, prevention
strategies for contacts.
Follow for at least 6 months to determine
if chronic infection develops.
Monitor ALT, HBsAg and anti-HBs.
If chronic infection develops, assess as discussed in chapters 7 and 10.
1. Notication.
2. Contact-tracing. Offer
testing. Vaccinate as
required. Education and
prevention strategies.
Follow for at least 6 months to determine if
chronic infection develops. Monitor ALT.
If ALT normal for 6 months, test HCV RNA
PCR to determine if virus has been cleared.
Legend Diagnosis
Management
Prevention
Diagnosis.
Treat for
specic
condition.
History and examination including epidemiological
and other clinical clues.
Cease any non-essential drugs that
may cause hepatitis.
Contact-tracing
Contact-tracing of individuals who may have been
exposed during the infectious period of acute
hepatitis should be undertaken to enable preventa-
tive measures to be implemented. Discussion with
the patient regarding how to proceed with contact-
tracing may be appropriate. The clinician may ask
the patient to consider recent blood-to-blood or sex-
ual contacts as well as recent blood donations. With
regard to HAV, household and occupational con-
tact-tracing may be relevant. Review of appropriate
State or Territory guidelines is recommended.
Public health notication
Cases of acute hepatitis are notiable by doctors
and diagnostic laboratories. Public health units
coordinate the response to outbreaks of hepatitis
and can provide advice on the appropriateness of
post-exposure prophylaxis for suspected contacts.
Opportunistic diagnosis and
prevention strategies
An episode of acute hepatitis should lead to risk
assessment and testing for other transmissible infec-
tions with similar routes of transmission (Chapters
13). The opportunity for implementing harm
reduction and preventative measures, such as vacci-
nation, should also be taken.
Specialist and/or hospital referral
Referral to hospital is appropriate in cases where
the primary care clinician assesses an individual to
have severe hepatitis or possible acute liver
failure. Specialist referral is recommended:
where the primary care clinician is unable to
make a denitive diagnosis;
where multiple diagnoses appear to co-exist;
for consideration of antiviral therapy in acute
hepatitis;
where other, treatable conditions have been
diagnosed.
Work
Persons with HAV infection are infectious for up
to a week after the onset of jaundice and should
not work. Workers in high-risk areas, for example
food handlers and childcare workers, should take
extended leave. Persons with acute HBV or HCV
infection do not need to be excluded from work if
they are clinically well, unless they are health care
workers who perform exposure-prone procedures
(Chapter 12). Further information may be
obtained from relevant State and Territory health
departments or medical registration boards
(Chapter 14).
Post-exposure management
The management of a person potentially exposed
to viral hepatitis will vary according to the nature
of the exposure, the available information about
the source of the exposure, knowledge of the
exposed persons immunity to viral hepatitis and
the time that has elapsed since the exposure.
Exposed individuals may self-present for
assessment or may be detected after contact-
tracing. As well as an assessment of the current
exposure, an assessment of future or ongoing risk
should be made and preventative strategies put
into place. In cases of workplace exposure to
hepatitis or potentially infected bodily fluids,
appropriate documentation should be completed
for workers compensation purposes.
Exposure to HIV as well as viral hepatitis
should be considered following exposure to blood
or bodily uids. See Chapter 4 for discussion of
HIV post-exposure prophylaxis.
Source status
Details of the sources clinical status should be
obtained where possible. Cases of clinically
apparent, acute hepatitis represent the most
straightforward category but cases of exposure to
bodily fluids from individuals without acute
hepatitis may be encountered. An assessment
should be made of risk factors for blood-borne
TABLE 5.3 Persons for whom hepatitis A vaccine
is recommended
6
Travellers to endemic areas
Visitors to rural and remote Aboriginal communities
Childcare and pre-school personnel
The intellectually disabled and their carers
Health care workers who provide care for substantial
populations of indigenous children
Sewage and waste disposal workers
Men who have sex with men
Injecting drug users
Persons with chronic liver disease
Persons with chronic HCV infection
should receive normal human immunoglobulin.
HAV vaccine can be commenced simultaneously
with normal human immunoglobulin and should
be considered for those at ongoing risk of HAV
infection.
6
HBV
Individuals who are HBsAg-positive (HBsAg+)
should be considered infectious. Non-immune
individuals with a denite HBV exposure through
heterosexual or homosexual sex, sharing of inject-
ing equipment, mother-to-child exposure or occu-
pational exposure (percutaneous, ocular, mucous
membrane exposure) should be given HBIG as
soon as possible within 48 hours. (The dose of
HBIG is 400 IU for adults and 100 IU for children.)
Concomitantly, HBV vaccination should be inject-
ed at a separate site and a full course completed.
HCV
No post-exposure prophylaxis against HCV
infection is currently available.
Post-exposure follow-up
After exposure to HAV, no specific serological
testing is required. Clinical follow-up is sufcient.
For HBV and HCV, the aim of initial follow-
up is to detect the development of acute or chronic
infection. Serological follow-up after exposure to
HBV and HCV should occur at one, three and six
months as both infections can have prolonged
incubation periods.
The HCV RNA PCR assay is currently funded
such that a single test can be undertaken for the
diagnosis of acute HCV infection. Additional test-
ing may be performed at the expense of the
patient. Most cases are viraemic at four weeks,
although some may have transient viraemia that
clears before this time. A single negative HCV
RNA result does not exclude infection with HCV
and full serological follow-up represents the cur-
rent gold standard of diagnosis.
Psychosocial issues
In managing patients who report potential expo-
sure to viral hepatitis or patients who present with
symptoms of acute viral hepatitis, a range of psy-
chosocial issues may be addressed in a timely and
sensitive manner. For example, risk behaviours
may be explored and appropriate referral to com-
munity support or counselling services offered
(Chapter 14). The anxieties and concerns of the
viral infections in the source. If the source is avail-
able and willing, screening for viral hepatitis and
HIV should be conducted with full pre-test and
post-test counselling.
In cases where the source has a history of
HBV infection, an urgent assessment of HBsAg
status will guide decisions regarding infectivity
and hence recommendations regarding post-
exposure prophylaxis.
Knowledge of the sources HCV status does
not change immediate management, as post-
exposure prophylaxis is not currently available.
However, the infectivity of a source that is repeat-
edly negative for HCV RNA in serum is probably
negligible.
5
Exposed persons immunity
After exposure to HAV, no specic tests of immu-
nity are undertaken. Prophylaxis is given to all
close contacts.
After exposure to HBV, an urgent assess-
ment of the exposed persons immunity is
required. This entails a history of previous HBV
infection or immunisation and response to vac-
cination. If the history is unclear, or response to
previous immunisation is unknown, then tests
to ascertain immunity to HBV may be under-
taken if the results can be obtained rapidly.
Administration of hepatitis B immunoglobulin
(HBIG) should not be delayed beyond 72 hours.
Check anti-HBc (as a marker of previous infec-
tion) and anti-HBs (if assessing response to
immunisation). If such tests are not available
within this time frame, the person should be
assumed to be non-immune.
Post-exposure prophylaxis
HAV
Post-exposure prophylaxis is recommended for the
close contacts of people with HAV. This includes
household and sexual contacts who have had con-
tact with the index case two weeks before, or up to
one week after, the onset of jaundice. Normal
human immunoglobulin is recommended and
should be given within two weeks of the exposure.
The standard dose is 2.0 ml (1.0 ml for persons
2550 kg; 0.5 ml for persons under 25 kg in
weight). It is given as a single intra-muscular injec-
tion. If the patient is a food handler, all other food
handlers at his/her place of work should receive
normal human immunoglobulin. If the patient is a
childcare worker, then unvaccinated co-workers
patients regarding transmission to sexual partners
and family can be addressed by a discussion of
modes of transmission and preventative strategies
(Case study 1, Chapters 2 and 3). Describing poten-
tial health outcomes, as well as the process of deter-
mining infection status, also may assist the patient.
Prevention
Prevention of perinatal transmission
Newborn babies of HBV-infected mothers should
receive HBIG and be started on a course of HBV
vaccination at birth. This strategy effectively pre-
vents transmission of HBV infection. There are no
effective strategies to prevent perinatal transmission
of HCV, although avoidance of invasive foetal
monitoring may be important. Potential benets of
caesarean section have not been proven and there is
no place for routine caesarean sections in HCV-
infected mothers. Breast-feeding is regarded as safe
unless blood is present in the milk.
Immunisation
6
HAV vaccination is recommended for some
populations at high risk (Table 5.3). Screening for
TABLE 5.4 Persons for whom hepatitis B vaccination
is recommended
6
TABLE 5.5 Serodiagnosis of acute and chronic viral hepatitis
Interpretation anti-HAV anti-HAV HBsAg anti-HBs anti-HBc HBeAg anti-HBe HBV DNA anti-HCV HCV PCR
IgM total IgM total
Acute hepatitis A +
Past hepatitis A +
Acute hepatitis B + + + or +
Acute liver failure - + or + + or + or
hepatitis B
HBsAg carrier + + +
(non-replicating) T
Chronic hepatitis B + + or + + +
(replicating) T
Previous (resolved) + or + +
hepatitis B
Recent HBV vaccination +
Acute hepatitis C + or +
Chronic hepatitis C + +
(symptomatic or
asymptomatic)
Resolved hepatitis C + or
Note: coinfection or superinfection may make interpretation more complicated.
Infants and young children
Young people aged
between 10 to 13 who
have never received a
primary course of HBV
vaccine
HIV-positive individuals
and other immuno-
suppressed adults
Liver transplant recipients
Household contacts of
people with acute HBV or
HBV carriers
Sexual contacts of people
with acute HBV or HBV
carriers (these people
should also be offered
hepatitis B immunoglobulin)
Men who have sex with men
Injecting drug users
Haemodialysis patients
Persons with clotting
disorders who require
multiple blood product
administration
Persons with HCV infection
Residents and staff of
facilities for persons with
intellectual disabilities
Inmates and staff of long-
term correctional facilities
Health care workers with
direct patient or human
tissue contact
Embalmers
Individuals adopting
HBsAg+ children
At-risk emergency services
personnel, police and waste
disposal workers
immunity prior to immunisation is recommended
for persons born before 1950, for those who
spent their childhood in endemic countries
(China, South East Asia and Pacic countries) and
for those who report previous hepatitis. The rec-
ommended schedule is an initial dose with a
booster dose 612 months later.
Since 2000, the HBV vaccination has been
available in Australia to all newborns and it is rec-
ommended for all children of 1013 years who
have not received a primary HBV vaccination.
Once there is serological evidence of a response to
immunisation, no further testing is required in
immunocompetent persons and boosters are no
longer recommended. HBV vaccination is also
recommended for populations at high risk
(Table 5.4). Vaccination is safe for people with
HIV, although protection is likely to be weak or
transient compared with the highly effective, pro-
tective immunity produced among immunocom-
petent individuals.
The recombinant HBV vaccine entails an initial
dose followed by two further doses at one and six
months. The vaccination schedule may vary
according to likelihood of compliance. The rapid
schedule (0, 7 and 21 days) may be more appropri-
ate in highly mobile populations.
6
Access to free
HBV vaccination is available through sexual health
clinics, some councils and other selected clinics.
A combined vaccine for HAV and HBV is
available and should be considered for individuals
at risk of both infections and for people with
chronic HCV. Such persons may include health
care workers and students, long-term visitors to
endemic countries, men who have sex with men,
injecting drug users, prisoners and prison workers.
There is no vaccine for HCV.
Education and harm minimisation
Education about risk reduction and harm minimi-
sation methods may lower the incidence of hepatitis
in at-risk individuals. Chapter 3 discusses preven-
tion and harm reduction messages.
Concurrent assessment for drug treatment
programs may be considered for those who inject
drugs. Referral to injecting drug user groups (such
as the Australian IV League or local equivalent)
for education and support may also be considered
(Chapter 14 ).
Travellers require accurate advice and appro-
priate vaccination or passive immunisation prior
to travelling to endemic areas.
Hand-washing is important to prevent trans-
mission of HAV.
Summary
The primary care clinician has a key role in identi-
fying cases of acute hepatitis and facilitating the
clinical monitoring and management of infected
individuals. Specialist referral is advised if signs of
acute liver failure develop or the diagnosis is
unclear. Following a possible exposure to viral
hepatitis or a diagnosis of acute viral hepatitis,
prevention measures and harm minimisation
strategies should be fully explored to reduce
ongoing transmission.
References
1 National Centre for HIV Epidemiology and Clinical
Research (NCHECR). HIV/AIDS, viral hepatitis and
sexually transmitted infections in Australia. Annual
surveillance Report 2003. Sydney: NCHECR; 2003.
2 Law MG, Dore GJ, Bath N, et al. Modelling hepatitis C
virus incidence, prevalence and long term sequelae in
Australia, 2001. Int J Epidemiol 2003;32:717-724
3 Alter HJ and Seef LB. Recovery, persistence and
sequelae in hepatitis C infection: a perspective on
long-term outcome. Sem Liver Disease 2000;20:17-35.
4 Quin JW. Interferon therapy for acute hepatitis C
viral infection: a review by meta-analysis. Aust NZ J
Med 1997;27:611-617.
5 Dore GJ, Kaldor JM, McCaughan GW. Systematic
review of the role of the polymerase chain reaction
in dening infectiousness among people infected
with hepatitis C virus. BMJ 1997;315:333-337.
6 National Health and Medical Research Council.
The Australian Immunisation Handbook. 8th edn.
Canberra: Department of Health and Aged Care;
2003.
deciency which had been identied in clusters.
The original case definition of AIDS has been
modied somewhat over the years but it remains
a list of conditions, now rare in the Australian set-
ting, that are seen predominantly in people who
present late with untreated HIV infection (Table
6.1). AIDS remains notiable in Australia, but the
prognostic signicance is less important in treated
populations than other markers of HIV, such as
CD4 cell count and viral load (Chapter 9).
Many HIV specialist clinicians and HIV-
infected people now favour such terms as early and
late HIV disease rather than AIDS. Alternatively,
clinicians may describe patients in terms of their
surrogate markers and clinical status.
When should HIV be considered
in the differential diagnosis?
The focus of this chapter is on specic clinical ill-
nesses, laboratory abnormalities and aberrant
responses to therapeutic interventions which may
indicate HIV infection as a differential possibility
to the astute clinician. Some of these clinical clues
are tabulated in Table 6.2. Whenever HIV anti-
body testing is recommended, there should be an
awareness of the psychosocial impact of testing
and full pre-test counselling should be undertaken
(Chapter 8).
A differential diagnosis of HIV may be con-
sidered in individuals who report exposure risks
for HIV infection during general health assess-
ments. Testing for HIV is commonly part of man-
agement of pregnant women and as part of
screening for sexually transmissible infections
(STIs). HIV antibody screening is performed at
blood, tissue and organ donation, prior to mili-
tary service and may be requested for some visas
and work permits. Consideration should be given
to HIV infection amongst other risks for
6
Signs and symptoms of
chronic HIV disease
Gary Rogers General Practitioner, Care and Prevention Programme, Department of General Practice,
Adelaide University, South Australia.
Anne Mijch Infectious Diseases Physician, Infectious Diseases Unit, Alfred Hospital, Prahran, Victoria.
Alan Brotherton Manager, Information Services and Gay Mens Health, AIDS Council of South Australia,
Norwood.
Introduction
Since the mid-1990s, the clinical manifestations of
chronic HIV infection have changed dramatically
amongst people with access to combination
antiretroviral therapy.
1,2
This chapter covers the
classical signs and symptoms of unmodied HIV
disease that can provide a basis for an initial
clinical diagnosis. It also discusses the clinical
issues seen in the large proportion of HIV-infected
people who are now taking combination anti-
retroviral therapy.
Acquired Immunodeciency Syndrome (AIDS)
was characterised in the early 1980s before HIV
had been identified. The Centers for Disease
Control (CDC) in the United States listed a group
of secondary conditions that suggested immuno-
Key points
Clinical diagnosis of HIV infection requires consideration of
HIV aetiology in relation to a range of sub-acute, chronic and
acute clinical presentations.
Chronic symptoms of immune activation (e.g.
lymphadenopathy, night sweats, fever) may indicate HIV
infection.
Mild, HIV-related immune deciency may be indicated by
persistent oral or skin conditions.
Laboratory markers such as thrombocytopenia, neutropenia
and lymphopenia may suggest HIV infection.
The incidence of classical AIDS-dening illnesses has fallen
dramatically in Australia since the introduction of combination
antiretroviral therapy. These conditions are now most common
among patients with advanced HIV disease whose HIV status
has been undiagnosed.
Combination antiretroviral therapy has dramatically altered the
course of clinical HIV disease. Immune reconstitution illness
and treatment-related side-effects are now common causes of
clinical symptoms.
immunosuppression prior to live viral vaccina-
tions, at consideration of transplantation and
when prescribing immunosuppressant medica-
tions. The assessment of HIV risk and subse-
quent counselling and management of the patient
are detailed in Chapters 2, 3 and 8.
Immune activation symptoms
primary infection
The acute retroviral syndrome characteristic of
primary HIV infection includes prominent fea-
tures of immune activation, such as fever, night
sweats, myalgia, arthralgia and lymphadenopathy
(Chapter 4). For a proportion of HIV-infected
individuals, these symptoms continue chronically,
indicating high-level immune system activity.
Clinical latency
The long phase of clinical latency that follows pri-
mary HIV infection conceals substantial virological
and immunological activity.
3
Some HIV-infected
people are able to control HIV replication and to
maintain CD4 cell levels for an extended period;
they are known as slow progressors or long-term
non-progressors. A small but signicant proportion
of people with HIV have been infected for close to
20 years but still have low viral loads and near nor-
mal immune function. For most untreated HIV-
infected people, however, there is a gradual decrease
in CD4 cell numbers over a period of 510 years,
when clinical HIV disease becomes apparent.
Mild immunodeciency
A variety of infectious agents can become more
troublesome relatively early in the course of
unmodied HIV infection when the CD4 cell count
falls below 500 cells/l (Tables 6.13). Most of
these are other chronic viral infections and the
appearance of clinical disease in HIV-infected
people is usually due to re-activation of latent
virus rather than new infection.
Shingles
An episode of classical herpes zoster can often
occur quite early in the course of chronic HIV
infection, particularly after another illness such as
a respiratory infection. It can be managed effec-
tively using aciclovir, valaciclovir or famciclovir.
Admission to hospital for intravenous aciclovir
may be warranted for those with severe pain or
multi-dermatomal or disseminated herpes zoster.
Herpes simplex
Orofacial and anogenital herpes simplex out-
breaks occur more frequently in HIV-infected
people. These may be extensive and persistent. In
people with more advanced disease, the ulcers
often coalesce, especially around the anus, to form
large, extremely painful ulcers. Herpes lesions con-
tinuously present for more than a month were part
of the original case denition for AIDS. However,
the advent of effective treatment for the herpes
simplex virus (HSV) means that chronic herpes is
now rare. Recurrent or persistent herpes may be a
sign of HIV infection in undiagnosed patients and
may be a trigger for risk assessment and further
physical examination.
Kaposis sarcoma
This malignancy, which in the days before HIV
was seen only in elderly men, is now known to be
TABLE 6.1 AIDS indicator diseases
Candidiasis (oesophagus)
Cryptococcosis (invasive)
Cervical carcinoma (invasive)*
Cryptosporidiosis with diarrhoea > 1 month
Cytomegalovirus of retina, brain, spinal cord, gastrointestinal
tract
Herpes simplex mucocutaneous ulcer > 1 month
HIV-associated dementia, disabling cognitive motor
dysfunction
HIV-associated wasting loss >10% body weight plus diarrhoea,
weakness and fever > 30 days*
Isosporiasis with diarrhoea > 1 month*
Kaposis sarcoma
Lymphoma, brain or non-Hodgkins (B-cell or immunoblastic)
Mycobacterium avium or kansasii (disseminated)
Mycobacterium tuberculosis disseminated or pulmonary*
Pneumocystis carinii pneumonia
Pneumonia (recurrent bacterial) *
Progressive multifocal leukoencephalopathy
Salmonella septicaemia (non-typhoidal, recurrent)*
Toxoplasmosis (brain)
* Requires HIV diagnosis.
caused by human herpesvirus type 8 (HHV8).
HHV8 appears to be sexually transmitted.
Additionally, high levels of virus have been
demonstrated in saliva. In Africa, horizontal trans-
mission among children may be important. In
Australia, Kaposis sarcoma (KS) is a sign of HIV
infection, especially in healthy men.
Kaposis sarcoma is most commonly manifested
as purple, nodular lesions on the skin or oral
mucosa (Figure 6.1) but can occur in visceral organs
such as the lungs and the gastrointestinal system.
Unpleasant or unsightly local tumours are
amenable to local therapy, intralesional chemother-
apy or palliative radiotherapy. For progressive
disseminated disease, systemic chemotherapy is
often benecial but the mainstay of management
involves restoration of immune function by con-
trolling HIV replication through antiretroviral
therapy.
Anogenital warts and squamous dysplasia
Anogenital warts are common in HIV-infected
people and usually represent re-activation of a
previous viral infection of the skin with the human
papillomavirus (HPV). In patients without an HIV
diagnosis, anogenital warts, especially recurrent
warts, indicate the need for HIV risk assessment
and further examination.
Anal or genital warts in the presence of HIV
infection may be conservatively managed, partic-
ularly if the person is considering the institution of
antiretroviral therapy for HIV. Warts often regress
spontaneously when immune function is restored.
Standard methods of treatment may be
employed. In the case of surgically removed anal
warts, biopsy tissue should be sent for
histopathology. Squamous dysplasia is often seen
and indicates that close follow-up is required.
There is some evidence to suggest that squamous
carcinoma of the anal canal is more common in
people with HIV and is probably related to HPV
infection.
Cervical carcinoma is significantly more
prevalent in women with HIV and is also proba-
bly related to HPV infection. It is generally
recommended that Pap smear cytology be per-
formed every 612 months in this group, with
management of abnormalities undertaken accord-
ing to the usual approach.
Molluscum contagiosum
These nodular lesions with a central punctum
commonly occur on the face, neck or anogenital
area. Although it does occur in non-HIV-infected
TABLE 6.2 Alarm bells suggestive of HIV infection
Clinical conditions where HIV should be considered
Oral candidiasis (especially in the absence of antibiotic use)
Atypical mononucleosis syndrome (not EBV- or CMV-related)
Aseptic meningitis with severe systemic symptoms
Difcult to manage psoriasis, dermatoses
Tuberculosis
Non-Hodgkins lymphoma
Cerebral space-occupying lesions
Persistent lymphadenopathy and symptoms of immune activation
Chronic vaginal thrush
Laboratory abnormalities where HIV should be considered
Thrombocytopenia, neutropenia, lymphopenia without cause
Anergy unexplained
Hypergammaglobulinemia new or unexplained
Therapeutic responses where HIV should be considered
Pneumonia unresponsive to standard therapy
Recurrent antibiotic-associated rash
FIGURE 6.1 Kaposis sarcoma
6 Signs and symptoms of chronic HIV disease
individuals, persistent appearance of molluscum
contagiosum in adults should lead to considera-
tion of HIV infection. Molluscum contagiosum
is caused by a poxvirus and, in HIV-infected individ-
uals, its incidence and severity relate to the degree
of immunosuppression. The condition is diag-
nosed clinically. Differential diagnosis in the HIV-
infected patient would include cutaneous crypto-
coccosis infection and, in individuals from South
East Asia, infection with Penicillium marneffei.
Lesions commonly regress with immune recovery
due to antiretroviral therapy or may be controlled
with local therapy.
Dermatoses
Rashes are common in HIV-infected people at any
level of immune function. Persistent, new or unusu-
al skin conditions may be the rst symptom of HIV
infection. The clinician should be alert to the possi-
bility of HIV infection and undertake a full risk
assessment and physical examination if extensive,
atypical or persistent rash is encountered.
The most common form of rash associated
with HIV infection is seborrhoeic dermatitis
(Figure 6.2) which is seen in most people at some
stage in the disease. It occurs at the classical sites
of scalp, ears, eyebrows, chest, axillae, groins and
feet. Standard treatment with steroid creams or
topical ketoconazole is often effective at control-
ling the problem but recurrence is usual. This con-
dition generally improves dramatically when
effective antiretroviral treatment is instituted.
Dermatophyte infections are also very com-
mon and can sometimes be difcult to differenti-
ate from seborrhoea. These infections can be very
extensive, particularly on the feet, and secondary
bacterial infection is common. Misdiagnosis of a
dermatophyte infection leads to ineffective treat-
ment with steroid creams that may in turn modify
the clinical appearance of the condition.
Other puzzling rashes are often seen in people
with HIV infection. Early skin biopsy may be a
useful guide where response to simple therapy is
inadequate. Eosinophilic pustular folliculitis is
one such pruritic papular condition that com-
monly occurs on the upper arm and chest for
which phototherapy has induced response in
many patients. Antiretroviral therapy often leads
to resolution of dermatoses.
Psoriasis occurs in people with HIV infection
with the typical erythematous scaly lesions occur-
ring over elbows, hands and feet. The guttate
form is also common. Pre-existing psoriasis can
be exacerbated by HIV infection and newly diag-
nosed psoriasis also has been described. Immune
recovery has been shown to improve these psori-
atic lesions in HIV-infected individuals.
Oral conditions
A condition called oral hairy leukoplakia is com-
monly seen prior to serious HIV-related oppor-
tunistic infections. It is manifest as distinctive
white areas on the lateral margins of the tongue
that cannot be rubbed off with gauze (unlike can-
didiasis). Its aetiology remains unclear although
one theory is that oral hairy leukoplakia is a man-
ifestation of mucosal Epstein-Barr virus (EBV)
infection. The condition is almost pathognomonic
of HIV infection and will sometimes prompt the
consideration of HIV testing when noticed by an
astute dentist or medical clinician at routine
examination.
Oropharyngeal candidiasis becomes more com-
mon in HIV disease when immunosuppression
occurs. Often it has the classical appearance of
cheesy plaques that can be rubbed off; occasionally,
it is subtler with an area of slightly furry redden-
ing, particularly on the palate. Candidiasis is
much less common in HIV-infected individuals
who are taking effective antiretroviral therapy.
Mycological examination of a wet swab will con-
firm the diagnosis. Treatment is only required
when the condition is symptomatic, and topical
amphotericin lozenges will often be effective for
mild disease. If the disease is more severe and
persistent, a course of uconazole capsules will
usually control it for a period.
Aphthous mouth ulcers appear to be more
common and more persistent in people with HIV
than among the HIV-negative population. These
ulcers may be quite large and are painful. When
simple measures are ineffective, topical steroids
appear to be benecial in a proportion of patients
and, in very severe cases, thalidomide may be use-
ful with appropriate precautions.
A particularly aggressive form of gum disease,
known as acute necrotizing ulcerative gingivitis
(ANUG), is commonly seen in the months before
FIGURE 6.2 Seborrhoea
clinical progression of HIV. Skilled care from a
dentist who is sensitive to the needs of HIV-
infected people is required if loss of otherwise
healthy teeth is to be avoided. Once again, the
condition is likely to abate signicantly with the
commencement of effective antiretroviral therapy
for HIV infection. Severe gingivitis may be sugges-
tive of possible HIV infection and may prompt
further enquiry in the undiagnosed patient.
Hepatitis coinfection
As other HIV-related opportunistic infections are
prevented or controlled, liver disease secondary to
coinfection with HBV or HCV and liver toxicity
from antiretroviral agents have become more
prominent. Coinfection may cause difculty toler-
ating HIV antiretroviral therapy, especially in the
initial immune reconstitution phase when hepatic
transaminase levels may rise. Close monitoring of
liver function is required at this time.
4
The presence of HIV leads to more aggressive
HCV disease and higher HCV viral load, and the
use of interferon and ribavirin in coinfected peo-
ple is currently being investigated. Careful moni-
toring of liver function tests and markers of HCV
infection (polymerase chain reaction and geno-
type), and avoidance of other hepatotoxins, such
as alcohol, is recommended (Chapters 9 and 10).
In the HIV-infected person, infection with
HBV may be associated with ares of hepatitis
during immune deciency, especially if lamivudine
(which is active against both HIV and HBV) is
withdrawn. Optimal management of HIV/HBV
coinfection has not yet been dened.
Immune reconstitution disease
In untreated people with advanced HIV infection
(CD4 cell count below 100 cells/l), marked
immunodeficiency inhibits the inflammatory
response that would normally occur to a variety
of infectious agents such as cytomegalovirus
(CMV), HCV and Mycobacterium avium. When
treatment reduces HIV viral load, there is rapid
restoration of the ability to mount inammatory
reactions. Consequently, infectious agents that
have peacefully co-existed with the host during
extreme immunodeciency are met with a marked
inflammatory response, and clinical disease
becomes apparent where few signs or symptoms
were evident previously (Figure 6.3). This phe-
nomenon has been named immune reconstitution
disease and was rst described by an Australian
team led by immunologist Dr Martyn French.
5
An
immune reconstitution illness is usually tempo-
rary because the inammatory effect is ultimately
successful at combating the infectious agent.
However, immune reconstitution illnesses can be
clinically signicant while present. In the case of
CMV retinitis, vision can be permanently impaired
by an episode of intense inflammation during
immune reconstitution.
When a patient presents with new symptoms
soon after starting antiretroviral therapy, immune
reconstitution should be considered as a possible
cause and appropriate referral and investigation is
advised.
Severe immunodeciency
More serious, life-threatening opportunistic infec-
tions generally appear when the CD4 count falls
below 200250 cells/l (Tables 6.13).
Pneumocystis
In the untreated person with HIV, Pneumocystis
carinii pneumonia (PCP) is often the rst serious
opportunistic infection. In the early days of HIV
management, PCP was often fatal. Risk of PCP
increases when the CD4 cell count falls below
about 200 cells/l. It is often insidious in onset
and typically presents as a persistent, dry cough
and exertional dyspnoea, sometimes accompa-
nied by mild-to-moderate constitutional upset
with fevers, sweats, lethargy and fatigue. If left
untreated, respiratory function can decline dra-
matically, leading to the need for ventilation and
intensive care management. The diagnosis can
often be made from the chest X-ray and is con-
FIGURE 6.3 Immune reconstitution and
Mycobacterium avium complex (MAC)
rmed by microbiological examination of sputum
induced by inhalation of nebulised hypertonic
saline.
The condition is now uncommon in people
with an HIV diagnosis because simple and effec-
tive prophylaxis is available. Double-strength co-
trimoxazole taken once daily by people with CD4
cell counts below 250 cells/l has dramatically
reduced the incidence of the condition.
In Australia and other countries where
antiretroviral therapy and PCP prophylaxis are
widely available, PCP is now most often seen in
people with longstanding, but undiagnosed, HIV
infection.
Mycobacterium avium complex (MAC)
Systemic infection with atypical mycobacteria is
commonly seen in people with CD4 cell counts
below 50100 cells/l. It produces a syndrome of
non-specic malaise, often accompanied by night
sweats, weight loss, anaemia and sometimes
respiratory or abdominal symptoms. Its symp-
toms merge with those of advanced HIV itself and
a high index of suspicion is required. MAC is an
important differential diagnosis of non-specic
fever in HIV-infected individuals (Table 6.3). The
diagnosis of MAC is confirmed by culture of
blood collected in special media. However, the
organism is slow to grow, so treatment with a
combination of anti-mycobacterial drugs is often
commenced presumptively. In those with epidemi-
ological risk factors, tuberculosis should be con-
sidered as a differential diagnosis and isoniazid
added to presumptive therapy until tuberculosis is
excluded.
Upon treatment, signicant clinical improve-
ment is usually seen and maintenance therapy is
continued indefinitely, unless marked and sus-
tained immune recovery is achieved with anti-
retroviral treatment. Effective prophylactic regi-
mens for MAC are now available. Azithromycin
given as a single dose of 1,200 mg weekly is most
widely used and is usually commenced when the
CD4 cell count is consistently below 100 cells/l.
Diarrhoeal diseases
Diarrhoea is an extremely common condition in
people with HIV infection.
Among patients with known HIV infection,
diarrhoea is often related to the adverse effects of
antiretroviral medication, particularly some pro-
tease inhibitors. When advanced immunodec-
iency is present (CD4 cell count below 100 cells/l),
opportunistic infections due to Cryptosporidium
and Microsporidium should be considered. Stool
examination is recommended if no obvious cause
for persistent diarrhoea is found in an HIV-infected
person. It is also important to ask the laboratory
to look specifically for parasites, such as
Microsporidium species, as this requires special
processing of the specimen. Colonoscopy and
mucosal biopsy may reveal CMV colitis in indi-
viduals with very severe immunosuppression.
Advanced HIV disease is associated with dia-
rrhoea and, if no specic cause is found after a full
diagnostic assessment, antidiarrhoeal agents such
as loperamide may be effective. The prolonged
use of quite high doses is not uncommon. Bulking
agents such as psyllium husk may also be useful.
Non-Hodgkins lymphoma
HIV-infected individuals have a 250- to 650-fold
increased risk of AIDS-related lymphoma over
the background population, with lymphoma
TABLE 6.3 Febrile syndromes in HIV-infected individuals
Differential diagnosis of undifferentiated fever in the HIV/AIDS patient
Current or nadir CD4 cell count < 200 cells/l Current or nadir CD4 cell count 200 cells/l
Disseminated Mycobacterium avium Bacterial infections, e.g. pneumonia, septicaemia
Pneumocystis carinii pneumonia Drug fever
Cryptococcal infection Tuberculosis
CMV infection Disseminated Salmonella, Campylobacter infection
Toxoplasmosis Fever associated with malignancy, e.g. lymphoma
Less common infections, e.g. Histoplasma, Bartonella
occurring most frequently in people with CD4
counts below 100 cells/l. Eighty-ve percent of
all AIDS-related lymphomas are systemic non-
Hodgkins lymphoma (SNHL), 15% are primary
CNS lymphoma (PCNSL), while primary effusion
lymphomas occur uncommonly. Almost all AIDS-
related lymphomas are high-grade diffuse large
B-cell (immunoblastic variant) or Burkitt's-like
lymphomas. EBV has a clear pathogenetic role in
PCNSL, a probable role in SNHL, and also may
be involved in primary effusion lymphoma where
HHV8 is implicated in disease pathogenesis.
Isolated enlarged lymph nodes, systemic febrile ill-
nesses and focal neurological abnormalities are
among the common presentations. Referral to
specialists in oncology and HIV-related malignan-
cies is recommended. Chemotherapy, radiother-
apy and combination antiretroviral treatment
provide the usual basis of therapy.
Neurological conditions
The direct effects of HIV on the brain can be evi-
dent at any level of immune function but may
become more prominent as the disease progresses.
Minor cognitive decits are quite common and, in
the absence of treatment, a signicant minority of
HIV-infected people will develop a clinical brain
disorder. In the early phase, this may manifest as a
syndrome that is almost indistinguishable from
mania, but a progressive, subcortical dementia
commonly evolves. The condition is characterised
particularly by extreme slowness of movement
and mentation which are severely disabling. HIV-
associated dementia often responds dramatically
to antiretroviral treatment, however the regimen
must be carefully chosen as only some of the
available agents penetrate the blood-brain barrier.
Space-occupying lesions of the brain also are
relatively common in people with advanced HIV
infection. The most likely diagnoses are primary
lymphoma of the brain and abscess resulting from
reactivation of toxoplasmosis. Toxoplasma abscesses
respond to appropriate antibiotic therapy, so early
diagnosis is important.
Other neurological conditions that were com-
mon in the days before combination antiretroviral
therapy are cryptococcal meningitis and progres-
sive multifocal leukoencephalopathy (PML).
Referral to an infectious diseases physician is
recommended when a neurological condition is
suspected in an HIV-infected patient.
Body composition changes
Weight loss and preferential loss of lean body
tissue is characteristic of progressive HIV infec-
tion and was common in people with AIDS in
the 1980s and early 1990s. Although this pic-
ture is still seen in people who are unable to tol-
erate antiretroviral medication, or where viral
resistance limits its effectiveness, most bodily
changes in HIV-infected people now appear to
be related to treatment.
Loss of facial and peripheral fat can be strik-
ing in people taking antiretroviral therapy,
creating a distinctive and easily identifiable
appearance (Figure 6.4). Patients may sometimes
complain first of varicose veins when their
healthy leg veins become more obvious as the
surrounding subcutaneous tissue is lost. The lat-
est research suggests that this syndrome may be
related in part to prolonged exposure to nucleo-
side analogue reverse transcriptase inhibitor
(NRTI) drugs.
6
FIGURE 6.4 Body composition changes
A proportion of HIV-infected people on therapy
also develop accumulation of fat in the abdomen
and sometimes the buffalo hump over the lower
neck posteriorly. Protease inhibitors are associat-
ed with marked dyslipidaemia in a high propor-
tion of patients and also may be involved in this
fat accumulation.
Psychosocial issues
In cases where clinical signs and symptoms lead to
an HIV diagnosis, consideration should be given
to the management of psychosocial concerns as
well as the clinical manifestations of the infection.
Post-test counselling and psychosocial follow-up
are fundamental following a positive HIV result
and issues for assessment and discussion may
include relationships, family, sex, work and dis-
closure (Chapters 8 and 9).
HIV-infected people now face a variety of seri-
ous challenges, including new manifestations of
HIV-related illnesses and medication-related toxi-
cities. While improved prognosis has led some
HIV-infected patients to reassess issues such as
education, work and relationships, difculty with
adherence to therapies and chronic toxicities have
in some cases led to a re-evaluation of lifestyle,
self-image or sense of wellbeing. In addition, the
challenges of living with a chronic or life-threaten-
ing condition, HIV infection itself and some med-
ications' side-effects may induce symptoms of
depression or anxiety which require acknowl-
edgement and management (Chapter 9).
Conclusion
Although the rate of HIV infection in Australia is
relatively low, the primary care clinician may give
consideration to HIV infection in relation to a
range of conditions, particularly when present in
young and otherwise healthy individuals. In the
age of combination antiretroviral therapy, clinical
diagnosis of HIV infection is likely to lead to
improved health and extended lifespan in the
patient.
While prescribing antiretroviral therapy requires
special training, many HIV-infected people also
visit general practitioners, who are ideally placed
to detect adverse developments at an early stage
and to facilitate optimal therapy. Chapter 9
addresses management of the HIV-infected
patient, particularly in regard to antiretroviral
therapy, psychosocial management, and support
and referral.
References
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2 Grulich A. Update: cancer risk in persons with
HIV/AIDS in the era of combination antiretroviral
therapy. AIDS Read 2000;10(6):341-346.
3 Ho D, Neumann A, Perelson A, et al. Rapid turnover
of plasma virions and CD4 lymphocytes in HIV-1
infection. Nature 1997;387:188.
4 Greub G, Ledergerber B, Battegay M, et al. Clinical
progression, survival and immune recovery during
antiretroviral therapy in patients with HIV-1 and
hepatitis C virus coinfection: the Swiss HIV Cohort
study. Lancet 2000;356:1800-1805.
5 John M, Flexman J, French MA. Hepatitis C virus-
associated hepatitis following treatment of HIV-
infected patients with HIV protease inhibitors: an
immune restoration disease? AIDS (US) 1998;12(17):
2289-93.
6 Carr A, Miller J, Law M, Cooper D. A syndrome of
lipoatrophy, lactic acidaemia and liver dysfunction
associated with HIV nucleoside analogue therapy:
contribution to protease inhibitor-related
lipodystrophy syndrome. AIDS 2000;14(3):F25-32.
Introduction
Acute infection with HBV or HCV can result in
chronic hepatitis if the infection persists for more
than six months. The rate of spontaneous clear-
ance varies according to the virus, the age at onset
of infection and other factors.
Spontaneous clearance of HCV generally
occurs during the rst year of infection in approx-
imately a quarter of infected individuals, with the
remainder developing chronic hepatitis. Although
gradual histological progression occurs in most
people, the condition is often asymptomatic for
an extended period of time. Symptoms arise with
the development of complications of advanced
liver disease but non-specific symptoms and
impaired quality of life are common among those
with earlier stages of liver disease. Cirrhosis
occurs in an estimated 1520% of people who
develop chronic HCV infection, 1540 years after
the original infection. Among those who develop
cirrhosis, liver failure occurs in 2030% and
hepatocellular carcinoma (HCC) develops in
1015% over 10 years.
1
Estimates of disease pro-
gression in hepatitis C are outlined in Figure 7.1.
The natural history of HBV infection is pri-
marily determined by the age of the individual at
the onset of infection. When acquired at birth or
during early childhood, the risk of development of
chronic infection is high, with only 2% of infants
spontaneously clearing the virus within three
years of infection and 15% clearing virus within
20 years. Among people with perinatally-
acquired HBV, 4050% of males and 15% of
females die from the liver-related causes.
2
In the case of adult-acquired HBV infection,
however, the situation is reversed with sponta-
neous clearance being the rule. Acute liver failure
occurs rarely, and only 35% of adults with acute
infection go on to develop chronic HBV infection.
In many cases, chronic HBV infection does not
result in symptoms or long-term problems
although 2030% of people will progress to
cirrhosis. These differences in outcome between
perinatal and adult-acquired infection are out-
lined in Figure 7.2. Of those with compensated
cirrhosis, 2030% will develop liver failure
(decompensated cirrhosis) and 1020% will
develop HCC over the next ten years. Survival
rates are high among those with compensated cir-
rhosis but much lower among those with liver
failure (85% versus 25% at ve years).
Symptoms and signs of
chronic viral hepatitis
Chronic viral hepatitis is frequently hidden due to
the asymptomatic nature of liver disease in a large
proportion of people and the slowness or absence
of progression to advanced liver disease. The
absence of symptoms and abnormal clinical signs,
therefore, does not exclude signicant liver dis-
ease. However, early diagnosis and treatment may
improve prognosis and, where appropriate,
patients should be offered treatment options.
7
Signs and symptoms of
Moira Sim General Practitioner, Yokine Family Practice, Mt Lawley, Western Australia.
Wendy Cheng Hepatologist, Royal Perth Hospital, Western Australia.
Greg Dore Infectious Diseases Physician, National Centre in HIV Epidemiology and Clinical Research,
University of New South Wales, Darlinghurst.
Kelly Beers HCV Educator, Hepatitis C Council, Perth, Western Australia.
Key points
The presence of signicant liver disease in patients may not be
apparent from symptoms or clinical examination. Conversely,
multiple symptoms in chronic hepatitis infection do not
necessarily mean the existence of signicant liver disease.
Progressive liver disease in chronic hepatitis B often involves
hepatic ares, whereas progressive disease is often
asymptomatic in chronic hepatitis C.
There is a poor correlation between biochemical and virological
markers of chronic viral hepatitis and symptoms and signs,
particularly in chronic hepatitis C.
Liver biopsy remains the denitive investigation for staging of
liver disease.
Although there is a great deal of
overlap, symptoms and signs of
chronic viral hepatitis can be divided
into those associated with:
early and/or slowly progressive
liver disease;
progressive liver disease;
advanced liver disease
complications;
extrahepatic manifestations.
In this classification, early and/or
slowly progressive liver disease
includes people with chronic hepatitis
C who progress slowly and may have
early brosis. Progressive liver disease
covers people who progress to cirrhosis
or, in the case of chronic HBV infec-
tion, have clinical evidence of progres-
sive disease such as hepatitis flares
but retain adequate liver function(e.g.
compensated cirrhosis).
Advanced liver disease complica-
tions includes people who have
developed clinical liver failure
(decompensated cirrhosis, e.g. hepatic
encephalopathy and failure of syn-
thetic function), portal hypertension
(e.g. ascites, oesophageal varices)
and/or hepatocellular carcinoma
(HCC). Extrahepatic manifestations
refers to a broad range of clinical con-
ditions associated with either chronic
hepatitis B or chronic hepatitis C.
Clearly these groups are not
mutually exclusive. For example, it is
possible to have progressive liver
disease and extrahepatic manifesta-
tions of chronic hepatitis. In addition,
there may be little clinical distinction
between early and/or slowly progres-
sive disease and progressive disease.
A long asymptomatic phase followed
by signs associated with cirrhosis or
decompensation is not uncommon.
Early and/or slowly progressive
liver disease
Symptoms of chronic viral hepatitis associated
with early and/or slowly progressive liver disease
are generally non-specic. Individuals frequently
complain of tiredness, anorexia, nausea, intoler-
ance to fatty foods, and abdominal discomfort,
particularly in the right upper quadrant region.
Others report general feelings of being unwell but
are unable to elaborate further. Fevers and night
sweats can also occur.
A number of recent studies have shown that
people with chronic HCV infection score poorly
on many quality-of-life parameters, including a
range of physical and psychological measures of
wellbeing. Again, these impairments are relatively
non-specic, and include reductions in general
health perception, mental health, physical
FIGURE 7.1 The proportion of HCV-infected persons who develop complications.
HEPATITIS C PROGRESSION
FIGURE 7.2 Prognosis according to age at onset of hepatitis B infection.
All hepatitis C infections
Chronic hepatitis C
Eventual symptoms/signs
of liver disease
Cirrhosis
Liver failure
Hepatoma
% of cases of chronic hepatitis
(percentage of infections) 20 40 60 80 100
100
0
Perinatally acquired Adult acquired
Age at onset of infection
Percentage of
infections
HEPATITIS B PROGRESSION
Chronic infection
Death from liver

disease
functioning, social functioning and vitality. These
measures may also be impaired in many people
with chronic hepatitis B. Successful clearance of
HCV through antiviral therapy has been shown
to improve quality-of-life scores.
The major feature of the symptomatology of
early and/or slowly progressive liver disease in
chronic viral hepatitis is its highly variable nature.
For many people, this stage of liver disease, which
may be the only stage they experience, is com-
pletely asymptomatic. On the other hand, many
people have considerable symptoms despite the
presence of mild liver disease or the absence of
biochemical evidence of liver inammation (nor-
mal ALT and AST levels). In fact, in chronic
hepatitis C there is little correlation between the
ALT level and presence of symptoms. Further-
more, the stage of liver disease (prior to liver fail-
ure) and the viral load in chronic hepatitis C have
a poor association with the extent of symptoms.
People with early or slowly progressive liver
disease generally have few clinical signs associated
with their chronic viral hepatitis. The most com-
mon clinical examination reveals either no abnor-
mal ndings or mild hepatomegaly. Presence of
peripheral stigmata of chronic liver disease, such
as multiple spider naevi and palmar erythema,
would generally indicate cirrhosis.
Progressive liver disease
Although the vast majority of people with chronic
viral hepatitis will not develop advanced liver
disease complications, many will eventually have
progressive liver disease. The symptoms covered
above may also be present in progressive liver
disease.
In chronic hepatitis B, particularly in the case
of perinatal or early childhood infection, a
prolonged asymptomatic period (immune toler-
ance phase) is followed by a more symptomatic
period (reactivation/clearance phase) in which
ares of clinical hepatitis may occur as the bodys
immune system attempts to clear infection.
2
These
ares are generally milder than an acute hepatitis
B clinical presentation, however, they often con-
sist of similar symptoms and signs. These include
lethargy, nausea, anorexia, food intolerance,
abdominal discomfort and jaundice. These clini-
cal ares in chronic hepatitis B are closely associ-
ated with biochemical evidence of increased
hepatic inammation. Marked elevations of ALT
and AST together with increased serum bilirubin
levels are often seen. A small proportion of people
each year in this reactivation/clearance phase will
TABLE 7.1 Factors associated with progression to
advanced liver disease in chronic hepatitis C
Age at acquisition of infection (>40 years)
Heavy alcohol intake (>40 grams/day)
Male sex
Longer duration of infection
Moderate to severe hepatic brosis on baseline liver biopsy
Coinfection with HIV and/or chronic hepatitis B
Obesity
Note: There is no evidence for an association between HCV viral load and
risk of disease progression.
7 Signs and symptoms of chronic viral hepatitis
FIGURE 7.3 Spider naevi in chronic hepatitis
FIGURE 7.4 Decompensated cirrhosis secondary to
hepatitis C
Prior to development of liver failure, there may be
little to distinguish a person with early or slowly
progressive liver disease from a person with pro-
gressive liver disease. If present, symptoms are
generally non-specic, as with early and slowly
progressive liver disease. Factors associated with
progressive liver disease in chronic hepatitis C are
listed in Table 7.1.
1,3
Peripheral stigmata of chronic liver disease,
such as spider naevi, liver nails and palmar eryth-
ema, may develop if there is progression to
cirrhosis. However, a completely normal clinical
examination may also be found in the presence of
cirrhosis related to both chronic hepatitis B and
hepatitis C.
seroconvert, initially from HBeAg-positive
(HBeAg+) to HBeAg-negative (generally with
development of anti-HBe) and subsequent loss of
HBsAg. People with frequent ares who have not
seroconverted may experience faster disease pro-
gression and are at high risk of cirrhosis and/or
HCC. Thus, people in this category should be
referred to a hepatologist or liver clinic for assess-
ment of stage of liver disease and possible thera-
peutic intervention. Antiviral therapy for chronic
hepatitis B is most efcacious during this period
through enhancement of clearance rates.
2
In chronic hepatitis C, clinical hepatitis ares
are rare and people often progress to cirrhosis
without development of signicant symptoms.
TABLE 7.2 Symptoms and signs of chronic viral hepatitis by stage of disease
Chronic hepatitis B Chronic hepatitis C
Symptoms Signs Symptoms Signs
Early and/or Generally none Often none Often none Often none
slowly Hepatomegaly Lethargy Hepatomegaly
progressive Anorexia
liver disease Nausea
Abdominal discomfort
Intolerance to alcohol
and fatty foods.
Progressive Often episodic Hepatomegaly Often none Sometimes none
liver disease Hepatic ares Mild jaundice Lethargy Hepatomegaly
Peripheral stigmata Anorexia Peripheral stigmata
of CLD* (palmar Nausea of CLD* (palmar
erythema, spider Abdominal discomfort erythema, spider
naevi, leuchonychia) Intolerance to alcohol naevi, leuoconychia)
if cirrhosis. and fatty foods. if cirrhosis
Advanced Increasing lethargy Peripheral stigmata Increasing lethargy Peripheral stigmata
liver disease Fluid retention of CLD* Fluid retention of CLD*.
Bruising Gynaecomastia Bruising Gynaecomastia
Prolonged bleeding Ascites/oedema Prolonged bleeding Ascites/oedema
Splenomegaly Splenomegaly
Distended abdominal Distended abdominal
veins veins
Bruising Bruising
Hepatic Hepatic
*CLD encephalopathy encephalopathy
chronic liver Jaundice (poor Jaundice (poor
disease prognostic sign) prognostic sign)
Advanced liver disease complications
Advanced liver disease complications of both
chronic HBV and HCV infection consist of liver
failure (decompensated cirrhosis), often in associ-
ation with signs of portal hypertension such as
refractory ascites and variceal bleeding, and
HCC. In chronic hepatitis C, HCC only develops
if there is underlying severe brosis or cirrhosis. In
contrast, as HBV itself is oncogenic, HCC can
develop in people with chronic hepatitis B with-
out signicant liver brosis.
Symptoms and signs of liver failure are the
same for chronic HBV and HCV, and are similar
to symptoms and signs associated with other
causes of decompensated cirrhosis. Consistent
with the underlying lack of synthetic function
(hypoalbuminaemia and coagulopathy), early
symptoms of liver failure may include ankle and
mild abdominal swelling, and easy bruising.
Increasing lethargy is generally also a feature.
Clinical examination should reveal some periph-
eral stigmata of chronic liver disease, as well as
some evidence of either peripheral oedema or
ascites. Later signs may include jaundice, which
indicates a poor prognosis in the presence of liver
failure, loss of hair and gynaecomastia. Clinical
evidence of portal hypertension may include
abdominal venous distension, splenomegaly and
ascites. Patients who have ascites may develop
spontaneous bacterial peritonitis (SBP). Patients
with unexplained fever or encephalopathy should
raise the suspicion of SBP and they should be
referred for diagnostic paracentesis. In addition,
the presence of peripheral neuropathy and cere-
bellar ataxia may suggest alcohol as a contribut-
ing cause of liver disease.
4
A history of haematemesis in a person with
other evidence of advanced liver disease suggests
the presence of oesophageal varices related to
underlying portal hypertension. Hepatic
encephalopathy also may be present in advanced
liver disease and may be subclinical in early
stages. A history of reversal of diurnal sleep pat-
terns, forgetfulness or inappropriate behaviour
may signal the onset of early hepatic encephalopa-
thy. Presence of either hepatic encephalopathy or
oesophageal varices indicates a poor prognosis.
Table 7.2 summarises the different signs and
symptoms related to stages of liver disease in
chronic hepatitis B and C.
Extrahepatic manifestations
Extrahepatic manifestations, although uncom-
mon, represent clinically important aspects of
hepatitis B and C. Specic treatment can be direct-
ed towards these conditions, some of which are
listed in Table 7.3.
Dermatological presentations include por-
phyria cutanea tarda (PCT), lichen planus and
vasculitic rashes associated with cryoglobuli-
naemia. These presentations should alert the clin-
ician to the possibility of chronic viral hepatitis. In
patients with PCT, which is typically associated
with chronic hepatitis C, blistered lesions, which
are exacerbated by exposure to the sun, occur on
the dorsum of the hands and forearms, and fer-
ritin levels are often mildly elevated. These
patients respond very well to venesection.
Rheumatological manifestations include
arthropathy, Sjogrens syndrome and polyarteritis
nodosa. A high serum globulin level, often associ-
ated with positive antinuclear antibody (ANA)
and rheumatoid factor, may indicate the presence
of cryoglobulinemia, which may be associated
with systemic complications such as glomeru-
lonephritis and vasculitis.
Other haematological abnormalities include
thrombocytopenia and leucopenia. Thrombo-
cytopenia may be the result of hypersplenism or
drug therapy, or it may be immune-mediated.
Neurological complications may be related to cryo-
globulinemia and present with mononeuritis of cra-
nial or peripheral nerves. Thyroid disease may be
subclinical. A variety of thyroid diseases have been
described in association with chronic viral hepati-
tis. Patients who test positive for ANA are more
TABLE 7.3 Extrahepatic manifestations of chronic hepatitis
Haematological Cryoglobulinaemia
Thrombocytopenia
Granulocytopenia
Renal Glomerulonephritis
Rheumatological Sjogrens syndrome
Polyarteritis nodosa
Arthropathy
Dermatological Lichen planus
Porphyria cutanea tarda
Endocrine Thyroid disorders
Neurological Mononeuritis
Peripheral neuropathy
prone to developing thyroid disorders, particularly
when treated with interferon. These thyroid disor-
ders, however, are generally reversible.
Assessment of the presence and
stage of disease
An assessment of the presence and stage of disease
often requires a step-wise investigation of serolog-
ical, virological, biochemical, ultrasonographic
and histological markers of viral hepatitis and
liver disease. In addition, clinical examination
may provide some indication of the stage of dis-
ease, particularly when advanced liver disease is
present. The results of these investigations may
determine access to antiviral treatment, which is
funded under Section 100 of the Pharmaceutical
Benets Scheme (Chapter 10).
Serological markers
In hepatitis C, a positive HCV antibody result
indicates prior or current infection but does not
distinguish between these two conditions.
In hepatitis B, serological testing provides use-
ful information on the presence of active infec-
tion. HBsAg is a marker of current infection. It
may disappear following acute infection or persist
in a person who remains a carrier. Anti-HBs
appears following the disappearance of HBsAg,
and is a marker of both naturally acquired and
vaccine-induced immunity. The presence of anti-
HBc IgM generally indicates recent infection since
it usually appears following acute infection and
disappears within a year. Occasionally, anti-HBc
IgM may be positive during hepatic ares in peo-
ple with chronic hepatitis B. Anti-HBc IgG can
persist indenitely following an infection, and sig-
nies exposure to HBV.
Most people exposed to HBV as adolescents
or adults clear the infection and will test anti-
HBc-positive (anti-HBc+) and HBsAg-negative.
HBeAg is a marker of viral replication and hence
infectivity. Anti-HBe generally develops as HBeAg
disappears, signalling resolution of acute infection
or cessation of replication. More complete clear-
ance of HBV infection is indicated by develop-
ment of anti-HBs.
2
Refer to Table 5.5 for a sum-
mary of serological and virological markers of
acute and chronic hepatitis.
Virological tests
HCV RNA testing by polymerase chain reaction
(PCR) can indicate the presence of HCV, as well
as viral load. A qualitative HCV RNA test gener-
ally distinguishes between a person who has
chronic hepatitis C and a person who has cleared
HCV either spontaneously or during treatment.
People who have cleared HCV will continue to
test positive for the anti-HCV but will be negative
for HCV RNA. Thus, if symptoms and signs of
active infection are present in a person with nor-
mal serum ALT levels who is HCV antibody posi-
tive and HCV RNA negative, a cause other than
hepatitis C should be sought.
On the other hand, the vast majority of people
with elevated serum ALT levels who test positive
for HCV antibody, particularly in the presence of
a risk factor for infection, have active infection
(viraemia). In these people, HCV RNA will be
positive and of no use in assessing the severity of
the disease. A quantitative HCV RNA or viral
load test does not provide information on the
stage of disease because there is little or no corre-
lation between the HCV viral load and the extent
of hepatic brosis or risk of disease progression
(in distinct contrast to the situation with HIV).
5
However, HCV viral load has some prognostic
value with regard to response to antiviral therapy,
and the HCV genotype is even more predictive of
response. HCV viral genotyping is helpful in
determining the likely response and optimal dura-
tion of antiviral treatment (Chapter 10).
HBV DNA is also a marker of active replica-
tion and can be assessed quantitatively to predict
likely response to antiviral treatment, with low
levels being associated with better outcome. The
vast majority of people who are HBeAg+ will be
positive on HBV DNA testing.
Liver function prole
The serum ALT level may give an indication of
hepatic inflammation although levels may be
normal despite progressive liver disease.
Nevertheless, people with either chronic HBV
or HCV who have consistently normal ALT levels
are at low risk of progression to cirrhosis.
6
Although people with abnormal ALT levels are at
increased risk of progressive liver disease, the level
of ALT in chronic hepatitis C is a relatively poor
predictor of disease stage and/or disease progres-
sion. In contrast, in chronic hepatitis B recurrently
high ALT levels generally indicate more active
underlying disease and risk of disease progression.
An inverted AST/ALT ratio (higher AST than
ALT) may indicate underlying cirrhosis in either
chronic HBV or HCV infection.
Albumin level (along with the prothrombin
time) gives an indication of the synthetic function
TABLE 7.4 Investigations in chronic hepatitis
Investigation Reason
HCV antibody (anti-HCV) Exposure to HCV.
HCV RNA PCR Detects presence of HCV.
HCV genotype Predicts response and optimal duration of treatment.
HBsAg Indication of natural hepatitis B infection. Occurs with acute infection and may
disappear or persist indenitely. Marker of ongoing infection (carrier).
Anti-HBs Indication of immunity to hepatitis B (from natural infection or vaccination).
HBcAg Found in the liver only and not usually measured.
Anti-HBc IgM Marker of recent exposure to hepatitis B virus. Does not persist more than a year
following acute infection.
HBeAg Indication of hepatitis B viral replication and high infectivity. Useful serological markers
in the investigation of a person who is found to be HBsAg+.
Anti-HBe Indication of hepatitis B viral clearance and occurs following loss of HBeAg.
HBV DNA Indication of viral replication. Quantitative level may help to predict response to
antiviral treatment (higher levels associated with poorer outcome) and monitor
response to treatment. Useful serological markers in the investigation of a person who
is found to be HBsAg+.
ALT Detection of abnormal ALT suggests antiviral treatment should be considered.
Albumin Indication of synthetic liver function i.e. low albumin indicates liver failure.
FBC Platelet counts may be low due to the progression of brosis or portal hypertension.
INR Indication of synthetic function.
HAV, HBV and HIV serology To determine need for vaccination to prevent superinfection with HAV and HBV.
Presence of HIV alters prognosis.
Thyroid function tests To exclude associated thyroid disorder and as a baseline investigation prior to
interferon treatment (which can cause toxicity).
Ferritin To exclude haemochromatosis (may reect severity of liver disease).
U&E and creatinine Baseline prior to treatment. To exclude possible renal involvement i.e.
glomerulonephritis.
Alpha-feto-protein Baseline investigation for hepatocellular carcinoma.
Caeruloplasmin and copper To exclude Wilsons disease.
Alpha-1-antitrypsin To exclude alpha-1-antitrypsin deciency.
ANA, SMA, LKM To exclude autoimmune disease.
Abdominal ultrasound To assess liver and biliary tree and to screen for hepatoma. Can also be useful to
detect small amounts of ascites.
Liver biopsy Denitive test for assessing severity of disease.
of the liver. Hypoalbuminaemia and prolonged
prothrombin time indicate decompensated cirrho-
sis. Recent evidence from a cohort of people with
chronic hepatitis C demonstrated that one of the
strongest prognostic measures is albumin level,
with higher rates of progression to liver disease
complications among people with levels below 35 g/l,
particularly if less than 30 g/l.
7
Liver imaging
Abdominal ultrasound is used to assess the liver
and biliary tree, as other causes of right upper
quadrant pain, such as gallstones, often need to be
excluded. In addition, abdominal ultrasound
helps to screen for HCC and to assess for small
amounts of ascites where doubt exists. However,
a normal ultrasound does not exclude cirrhosis
and this investigation is probably unnecessary in a
person with no clinical evidence of chronic liver
disease. Alpha-fetoprotein level should also be
measured at baseline, and monitored every six
months, especially in people with chronic hepatitis
B and those with cirrhosis, since this is a useful
marker of HCC.
Other investigations
Other tests are used to identify complications or
coexisting problems that may impact on prog-
nosis and treatment decisions. For example, a
low platelet count may signal the development
of portal hypertension and hypersplenism. The
presence of coexisting HBV, HCV or HIV may
alter prognosis and treatment options. In treat-
ing hepatitis C, HAV and HBV status should be
determined in order to offer vaccinations
against superinfection by these organisms,
which might worsen prognosis. Similarly, in
treating hepatitis B, vaccination against HAV
should be considered.
Thyroid function tests are useful to exclude
associated thyroid disorders. They also should
be conducted prior to antiviral therapy, which
has been known to cause toxicity to the thyroid
gland. Ferritin levels, alpha-1-antitrypsin, caeru-
loplasmin and copper levels are measured to
exclude the other hepatic pathologies:
haemochromatosis, alpha-1-antitrypsin decien-
cy and Wilsons disease. Antinuclear antibody
(ANA), anti-smooth muscle antibody (SMA)
and liver kidney microsomal antibody (LKM)
are markers for auto-immune liver disease.
Low titres of ANA and SMA may be present in
liver disease and may not indicate auto-immune
liver disease.
Liver biopsy
The denitive test for the assessment and staging
of disease is a liver biopsy.
8
Liver biopsy is usually
offered to patients with abnormal ALT levels who
may be considering antiviral therapy. It also great-
ly assists in determining prognosis over the short-
to-medium term. Patients are frequently fright-
ened of the invasive nature of this test. In addi-
tion, some patients mistakenly believe that they
will not receive pain relief if they disclose a histo-
ry of drug use. This should be addressed by
explaining that liver biopsy is the most accurate
way to assess the level of liver damage and by
offering information about the procedure itself
and the expertise of the people performing the
biopsy.
Patients are often puzzled because of the lack
of correlation between their symptoms, their
blood tests and the serious consequences that can
be associated with viral hepatitis. It is important
to stress that the absence of symptoms, signs and
abnormal ALT levels does not exclude signicant
liver damage.
A summary of the investigations used in
chronic viral hepatitis is provided in Table 7.4.
Clinical examination
Physical examination of patients with suspected
or conrmed viral hepatitis consists of general
inspection as well as attention to specic signs of
chronic liver disease and associated systemic
disorders. Examination should include:
general appearance and mental state of the
patient;
peripheral examination of the hands (for pal-
mar erythema, Dupuytrens contracture, leu-
chonychia, blistered lesions);
examination of the arms or trunk (for abnor-
mal bruising, spider naevi, loss of hair and
gynaecomastia);
inspection for jaundice, anaemia and parotid
enlargement;
inspection of the abdomen (for evidence of
collateral circulation, herniae, hepatomegaly,
splenomegaly and ascites);
signs of fever or encephalopathy;
peripheral neuropathy and cerebellar ataxia
(which suggest alcohol as a cause of liver
disease);
a history of reversal of diurnal sleep patterns,
forgetfulness or inappropriate behaviour
may signal the onset of early hepatic
encephalopathy.
Summary
Chronic hepatitis C and chronic hepatitis B are
generally asymptomatic and therefore frequently
hidden to both the patient and the clinician. Since
a history of risk behaviour is often not disclosed
to doctors, a reason to offer testing and diagnosis
may not present itself. When symptoms do occur,
they are largely non-specic and common symp-
toms that may be the result of a myriad of
diseases. Consequently, the diagnosis of HCV or
HBV infection can be easily missed. Being alert to
the possibility of chronic viral hepatitis as a cause
of many clinical presentations will allow early
diagnosis and the offer of treatment.
Blood tests and ultrasound imaging help to
assess hepatic function and the presence of complica-
tions and other associated disease that may be criti-
cal to decisions about prognosis and treatment.
However, a lack of symptoms and signs and normal
ALT levels does not exclude progressive damage in
chronic hepatitis. Liver biopsy is the denitive test to
identify the stage of liver disease.
Many patients who are aware that they may
have put themselves at risk of contracting HBV or
HCV are reluctant to seek a diagnosis, not only
because of fear of prejudice and hesitancy in fac-
ing a potential serious illness, but also because
they are pessimistic about treatment outcomes. It
is essential that clinicians present optimism, since
in recent years there have been substantial gains in
outcomes following treatment. Support groups
such as State and Territory Hepatitis C Councils
(Chapter 14) can be helpful in providing additional
resources to help present a more optimistic view
and give patients a better sense of control over
this chronic condition.
References
1 Seeff LB. Natural history of hepatitis C. Hepatology
1997;26(Suppl 1): 21S-28S.
2 Lee WM. Hepatitis B virus infection. N Engl J Med
1997;337:1733-1745.
3 Poynard T, Bedossa P, Opolon P, et al. Natural
history of liver brosis progression in patients with
chronic hepatitis C. Lancet 1997;349:825-832.
4 Bacon BB and Di Bisceglie AM. Viral Hepatitis:
Clinical features in liver disease: Diagnosis and
management. Churchill Livingstone;2000:79-97.
5 Thomas DL, Astemborski J, Rai RM, et al. The
natural history of hepatitis C virus infection: host,
viral, and environmental factors. JAMA
2000;284:450-456.
6 Marthurin P, Moussalli J, Candranel JF. Slow
progression rate of brosis in hepatitis C virus
patients with persistently normal alanine
transaminase activity. Hepatology 1998;27:868-872.
7 Khan MH, Farrell GC, Byth K, et al. Which patients
with hepatitis C develop liver complications?
Hepatology 2000;31:513-520.
8 Desmet VJ, Gerber M, Hoofnagle JH, Manns M,
Scheuer PJ. Classication of chronic hepatitis:
diagnosis, grading and staging. Hepatology
1994;19:1513-1520.
Introduction
Testing for HIV, HBV and HCV mandates pre-
test and post-test counselling. The aims of pre-test
and post-test counselling are to minimise the
personal impact of diagnosis, to change health-
related behaviour and to reduce anxiety, particularly
when the patient has not initiated testing.
Counselling thus requires the clinician to assess
risk, educate the patient regarding risk of trans-
mission, obtain informed consent and follow-up
and arrange referrals as indicated.
The context of testing
Testing for HIV antibody has been available in
Australia since October 1984. At that time, AIDS
was associated with high morbidity and mortality,
and an HIV diagnosis was highly stigmatised due
to its association with marginalised social groups.
HIV antibody testing was promoted primarily as
a tool to enhance education and prevention
initiatives. Since the mid-1990s, HIV treatment
advances have reduced the number of AIDS-related
diseases, AIDS notifications and AIDS-related
deaths.
1
The widespread availability of antiretro-
viral therapy in the contemporary Australian set-
ting has dramatically changed the medical context
of HIV antibody testing; an HIV diagnosis now
opens up the possibility of appropriate treatment
and improved prognosis. However, despite treat-
ment advances and changes in social perceptions,
HIV/AIDS remains a stigmatised condition and
all people who are tested should be given detailed
and sensitive pre-test and post-test counselling.
Testing for HCV antibody has been available
since 1990. As with HIV, HCV infection is stigma-
tised due to the association with injecting drug use.
During pre-test counselling, questions may be
asked about a history of injecting drug use that
may be an unwanted reminder of a past phase of a
persons life and may be resisted. However, a dis-
cussion of previous or present drug use provides
an opportunity to educate the individual about
HCV transmission and natural history. As with
HIV, the benets of testing include interventions
and treatments to improve clinical outcomes and
facilitation of measures to prevent transmission.
Long-term management of HBV infection has
changed due to the introduction of effective
antiviral treatment and immunisation. The avail-
ability of HBV vaccination enables clinicians to
take an active role in case-finding, leading to
lower rates of transmission and identication of
people with chronic HBV infection who may be
suitable for treatment. Widespread community
ignorance about the long-term complications of
chronic HBV infection (Chapters 1, 7 and 10) still
exists, and patients need to be suitably counselled.
8
Talking about testing:
pre-test and post-test counselling
Key points
Pre-test counselling is essential for the patient to make an
informed decision regarding HIV, HBV and/or HCV testing.
Pre-test counselling provides the person with information about
HIV, HBV and/or HCV, including modes of transmission and
how to prevent infection. It helps the person to consider the
implications of a positive result.
Pre-test counselling should be adapted to an individuals
knowledge and cultural understandings as appropriate. Testing
should not be avoided because pre-test counselling is too hard.
In positive individuals, post-test counselling explores support
and resources available to the patient and provides education
regarding the infection and how to minimise the risk of
transmission.
In negative individuals, post-test counselling provides information
on safe sex or injecting and addresses risk behaviour that led to
the possible exposure.
Paul Andrews Sexual Health Counsellor, Short St Centre, St George Hospital, Kogarah, New South Wales.
Katherine Fethers Head of Sexual Health, Alice Springs Hospital, North Territory.
Ron McCoy General Practitioner, East St Kilda, Victoria.
Paul Harvey Information/Resources Ofcer, Hepatitis C Council of New South Wales, Surry Hills.
Jenean Spencer Epidemiologist, Population Health Division, Commonwealth Department of Health and
Aged Care, Canberra, Australian Capital Territory.
Reasons for testing
HIV, HBV and HCV antibody testing is indicated:
upon patient request;
upon identication of clinical symptoms or
signs (Chapters 47);
upon identication of risk factors in the
patient history (Chapters 23);
as part of a screening process;
following a possible occupational or non-
occupational exposure to the blood or bodily
uids of a person whose infection status is
positive or unknown.
Screening may relate to antenatal testing, pre-
surgical testing, military requirements, blood
donation, and/or immigration or insurance
requirements. Regardless of the reason for test-
ing, pre-test counselling by the clinician and
informed decision-making by the patient are
essential.
Patients who request testing may not reveal
their full level of risk. In some situations, the clin-
ician may assess the risk of infection as low but
the patients actual risk of infection may be high.
For this reason, all patients requesting testing
should be tested. Some patients, for example
young people, may attend hoping to arrange an
HIV, HBV or HCV test but are unable to state this
request directly. In such cases, a request for a
check-up or blood tests may prompt question-
ing by the clinician to elicit specic concerns (Case
Study 1).
Other requests for testing may occur follow-
ing an exposure, either in a medical context or
occasionally in a public setting. Parents may pre-
sent with young children who have inadvertently
handled discarded syringes. In these circum-
stances, often the precise details of the exposure
are unclear and the risk is difcult to assess.
Legal requirements
Some States and Territories have specific legal
regulations relating to pre-test and post-test
counselling for HIV and viral hepatitis, which
may be used as a guide to minimum standards of
care. Contact the relevant State or Territory
health department for details (Chapter 14).
Chapter 13 contains further discussion of legal
responsibilities and highlights the need for full
documentation of recommendations, counselling
and follow-up undertaken by the clinician.
8 Talking about testing: pre-test and post-test counselling
The counselling process
During the counselling process, information is
exchanged and concerns explored. Coping strate-
gies are developed that may be utilised in the event
of a positive result. While discussion does not need
to proceed according to any formula, key informa-
tion areas need to be covered during the consulta-
tion (Table 8.1). Referring to a framework of key
points ensures that the necessary information
regarding blood-borne viruses is conveyed.
Within the context of general practice, clini-
cians may often recommend testing for HIV,
HBV and HCV but rarely see positive results,
particularly in relation to HIV. Consequently,
detailed pre-test counselling may seem unneces-
sary. However, testing usually occurs because
there is some level of risk and each case of testing
for blood-borne viruses needs to be taken seriously.
Pre-test counselling provides an opportunity for
the clinician to educate patients in risk reduction
while ensuring diagnostic vigilance is maintained.
TABLE 8.1 Summary of pre-test counselling
Motivation/reason for test
History of testing
Psychiatric status and assessment of social supports
Exposure/risk assessment
Condentiality
Natural history and transmission
Prevention of transmission
Implication of a positive or equivocal test result, including
availability of treatment
Implications of a negative test result
Explanation of the window period
Advice on disclosure to family and friends
Assessment of ability to cope with testing and possible
diagnosis
Support services
Logistics of the HIV test: time taken for results to become
available and the need to return for results
Pre-test counselling
Pre-test counselling has several objectives:
to provide information about the implications
of a positive or negative result;
to enable informed decision-making about
testing;
to communicate the health benets of testing;
to educate patients about safe sex and risk
reduction measures;
to prepare for a possible positive result.
History-taking and risk assessment
A non-judgemental counselling approach and a
climate of openness and trust encourages honest
answers to highly personal questions. Consideration
of actual risk practices, rather than making assump-
tions based on the patients perceived membership
of a particular risk group, is the accurate way to
perform a risk assessment. Chapter 3 addresses
sexual and drug-use history-taking in detail, and
Chapters 2 and 3 discuss risk assessment.
Issues to cover during pre-test
counselling
Table 8.1 lists topics to be addressed during pre-
test counselling. In particular, the following points
should be explored before the patient consents to
testing:
Condentiality
Advise the person of the measures the service or
practice takes to protect personal information,
including results, as well as public health notica-
tion requirements (Chapter 13).
Medical consequences of infection
Provide information about natural history and
modes of transmission for HIV, HBV or HCV
(Chapters 1 and 2 and Appendices).
Information about prevention
Discuss the relative risks of transmission of HIV,
HBV and HCV associated with various practices
(Chapter 2). Explore the persons ability to prac-
tice safe sex or safe injecting (Chapter 3).
The implications of a positive result
Inform the patient that the presence of antibodies
means viral infection has occurred. Discuss impli-
cations of chronic infection for sexual relationships,
the existence of treatments and the emotional and
social supports that infected people can access.
The benets of HBV immunisation for household
members and sexual partners may be relevant.
Some individuals may be reluctant to test even
when the availability of treatments has been
explained to them. They may believe that it will
be impossible to keep results private and they may
hold well-founded fears of discrimination, social
exclusion or personal violence that may follow
disclosure of HIV or viral hepatitis infection.
Implications of an equivocal result
Prepare the patient for the possibility of an equiv-
ocal result and the need to re-test.
The implications of a negative result
The absence of antibodies (the negative result)
means either the person is not infected or that
he/she is in the so-called window period of
infection, prior to the development of antibodies.
The window period may be as long as three
months from the date of initial exposure for HIV
and six months for HBV and HCV.
Coping with the results
Previous ways of coping with crises may indicate
how the person will cope with a positive test result.
People with a history of depression or other
psychiatric issues and those without self-perceived
social supports are especially vulnerable following
a positive diagnosis. Assess the patients psychi-
atric history and risk of suicide or self harm, and
identify appropriate interventions in the event of a
positive diagnosis. In cases where high-risk prac-
tices or clinical features are suggestive of infection,
in-depth discussion of these issues may form the
basis of a future management plan.
CASE STUDY 1
An adolescent may request testing indirectly
Indirect requests for testing
Mary is a 16-year-old girl who presents for a check-up and reports
feeling sick. Upon history and examination she is well but the
clinician decides to perform a full blood count and iron studies.
While the blood is being taken, Mary asks, By the way, doctor,
does this test for AIDS?. Subsequent assessment indicates that
Mary has had unprotected vaginal sex and is concerned about
sexually transmissible infections (STI). The clinician performs HIV
pre-test counselling and conducts a full STI screen including an HIV
test. A follow-up appointment is arranged and information provided
about the local youth service which provides targeted health
information.
Referral
The need for assistance from other agencies may
arise during this process and clinicians need to
have a low threshold for referral to specialist
agencies. For example, when assessing patients
with a history of injecting drug use, issues related
to homelessness, poverty or drug and alcohol
dependence may become apparent and referral
may be indicated (Chapter 14).
Supporting the person while waiting for
the result
Ensure that follow-up appointments are booked
at the pre-test assessment. Suggest that a trusted
person be told about the test if the patient requires
support while waiting for test results. In addition,
the patient may be invited to bring a support per-
son when returning for his/her result.
Summary
While pre-test counselling may seem time con-
suming, practice ensures that time is used effi-
ciently within the primary care context. Clinicians
will often develop their own style for discussing
HIV and viral hepatitis, tailoring information and
language to the needs of individual clients. Not all
of the issues listed above may be relevant to every
patient each time he/she presents for testing, but
assumptions regarding the patients level of
knowledge should be avoided. While the process
may seem unnecessary in low-risk patients, thor-
ough pre-test counselling ensures that prevention
measures are in place, the patient is prepared for
his/her test results, and the clinicians ethical and
legal obligations are met.
Post-test counselling
All HIV, HBV and HCV test results must be given
in person. Ensure privacy and undertake the con-
sultation in an area where you will not be inter-
rupted.
Giving a positive result
The following points, summarised in Table 8.2,
should be considered when providing post-test
counselling in the event of a positive HIV, HBV or
HCV test result.
Assess patient readiness to receive
result
The person may be asked whether he/she has
thought about the likely test result and its implica-
tions. If the person does not seem prepared,
relevant issues covered in pre-test counselling may
be reviewed. Alternatively, attendance may indi-
cate the patient is ready to hear the result and it
may be appropriate to give the result directly.
State the result clearly
Some people confuse a positive result with a
good result. Ensure that the actual result is clear.
Avoid information overload
Give the patient time to process and react to the
information. Listen and respond to the persons
needs.
Reinforce commitment to health care
The primary care clinician may reassure the
patient that he/she will continue to be a partner in
the patients health care without discrimination.
Enlist available supports
Help plan the persons next 2448 hours. Arrange
a follow-up appointment during the next two
days and offer an after-hours phone contact.
Discuss disclosure
After a positive result, the patient may experience
an urge to tell many people. The balance between
disclosure and privacy can be difcult, and the
clinician may caution the patient about widely
disclosing his/her positive status during the rst
few days after diagnosis, due to the possibility of
negative responses from some people.
Supply written material
Supplying written material gives the person some-
thing to read outside of the consultation, reinfor-
cing key messages that may not have been heard
in the context of the shock of receiving a positive
result. Information may address the medical and
social consequences of HIV, HBV or HCV infec-
tion and provide details about local support ser-
vices, including telephone information and sup-
port lines, AIDS Councils or Hepatitis C Councils
(Chapter 14). The ASHM website at www.ashm.
org.au can provide contact details and links.
Managing a positive result
Much of the initial management of a new blood-
borne virus diagnosis is psychosocial. Offering the
patient the opportunity to return at any time to
discuss concerns may help him/her to adjust to the
diagnosis.
Chapters 9 and 10 discuss initial and ongoing
assessment, monitoring and management of patients
with HIV and viral hepatitis.
Clinicians inexperienced in managing patients
with blood-borne viral infections should collabo-
rate with more experienced general practitioners
and/or relevant specialists and specialist centres
(Chapter 14 and the ASHM Directory).
Giving a negative result
The following points should be considered for dis-
cussion when providing post-test counselling for a
negative HIV, HBV or HCV test result (Table 8.3).
Inform the patient of the result
Tell the patient that he/she is not infected. If
appropriate, discuss the window period and make
an appointment for re-testing.
Educate the patient about ongoing
risk-taking
Review safe sex and safe-injecting practices.
Discuss the role of drugs and alcohol in risk-tak-
ing, as well as how and where to access condoms
and clean injecting equipment. Offer referral to
local services as appropriate (Chapter 14).
Offer vaccination
Hepatitis A and hepatitis B vaccination may be
offered.
Address attitudinal barriers
A negative result leaves time to explore important
issues that may impact on infection risk. For
example, a negative result after a high-risk
encounter may reinforce a sense of invincibility
amongst young people, especially young men.
Such responses need to be addressed.
Equivocal (indeterminate) results
Occasionally, an equivocal or indeterminate
result from HIV, HBV or HCV testing may
occur. This can be a source of great uncertainty
and anxiety for the patient. Clinicians need to
consult pathology laboratory staff or the
National Serology Reference Laboratory for
specialist advice in interpreting equivocal results.
Specic tests for each blood-borne virus have
different types of equivocal results and differing
rates of false positivity. In the case of HIV
antibody testing, a positive ELISA and a single
band on Western blot constitutes an equivocal
result.
A patient with an equivocal result who has
reported a recent high-risk exposure is regarded
as being in the window period of infection and
may require considerable support during this time
to deal with the uncertainty. Further tests for viral
antigens may be indicated to test for the presence
of infection and should be performed in consulta-
tion with a specialist clinician. Repeat HIV anti-
TABLE 8.2 Summary of post-test counselling:
giving a positive result
First post-test consultation
Establish rapport and assess readiness for the result
Give positive test result
Avoid information overload
Listen and respond to needs (the patient may be overwhelmed
and hear little after being told the positive result)
Discuss immediate implications
Review immediate plans and support
Reassess support requirements and available services
Arrange other tests and next appointment
Subsequent consultations
Treatment options, diet and exercise
Effect of diagnosis on relationships (HIV-infected people are
legally required to advise their sexual partners of their status)
Issues of disclosure
Travel to certain countries may be restricted for HIV-
infected individuals
Access to life insurance may be affected
Workplace implications
Impact of other issues (drug use, poverty, homelessness) on
ability to access health care and treatments
TABLE 8.3 Summary of post-test counselling:
giving a negative result
Explain negative test result
Reinforce education regarding safe behaviours
Consider vaccination for hepatitis B and hepatitis A
Further discuss anxiety or risk behaviours
body testing is generally offered at one month. If
seroconversion is suspected, an HIV proviral
DNA PCR assay may be used to determine HIV
status (Chapter 4). Repeat HCV antibody testing
may be offered using a different antibody test.
Alternatively, a PCR assay may be used in consul-
tation with a specialist centre to detect the pres-
ence or absence of virus.
A patient with high-risk behaviours, a history
of recent exposure, clinical signs and/or specic
types of equivocal results is at high risk of sero-
converting. Upon repeat testing, these people usu-
ally test positive.
In populations of low seroprevalence of blood-
borne viral infections, equivocal results may be
false positives. Factors such as pregnancy, past
blood transfusions, intercurrent viral infections,
autoimmune diseases and malignancies may play
a role in equivocal results. Upon re-testing at one
month, a second equivocal result is regarded as
conrmation of negative status.
Special considerations
Cross cultural issues
Culture, language, literacy level, gender and age
will affect how a person accepts and understands
HIV, HBV and HCV testing but this should not
interfere with provision of pre-test and post-test
counselling.
Language barriers may be overcome by the
use of an interpreter. Highlighting the need for
condentiality with the interpreter and reassuring
the patient may be appropriate. Nevertheless,
people of non-English speaking and indigenous
backgrounds may hesitate to communicate
through an interpreter due to fear that conden-
tiality will be breached. This may be particularly
relevant in rural and remote settings where the
interpreter may be closely connected with the
patients family.
Pre-test and post-test counselling may need to
be adapted to suit the needs of a particular cultural
group. In the Northern Territory, for example,
changes to traditional pre-test counselling
practices have occurred in conjunction with the
training of community-based, Aboriginal health
workers and the development of culturally
appropriate resources and videos in indigenous
languages. In addition, the term pre-test coun-
selling has been replaced by the term pre-test
information in an attempt to reduce clinician
anxiety about pre-test counselling and to nor-
malise HIV testing. However, any changes to
pre-test and post-test counselling protocols should
be undertaken in consultation with State or
Territory public health authorities and appropri-
ate specialist services or organisations.
HIV, HBV or HCV phobia
Occasionally the clinician will encounter an indi-
vidual whose fear of infection with HIV or viral
hepatitis is out of proportion with the actual risk
of infection. Such individuals, sometimes referred
to as the worried well, may repeatedly request
HIV or HCV tests after encounters that carry very
low or no risk of transmission. Often these people
are helped by emotional support or a discussion
of the encounter and the provision of factual
information about the risk of transmission. This
may not be adequate for some individuals who
may have co-existing psychiatric morbidity, such
as undiagnosed obsessive compulsive disorder,
and may need referral for specialist counselling or
psychiatric assessment.
HIV, HBV or HCV anxiety
Some people demonstrate extreme anxiety when
presenting for testing. This anxiety may be due to
behaviour, which the patient reports as out of
character, that has resulted in risk of exposure to
a blood-borne virus. For example, a married man
may report guilt and fear of infection following
protected sex with a sex worker. The anxiety may
arise from the mans actions and may be exacer-
bated by his thoughts about the real or imagined
interpersonal consequences of an infection, such
as divorce from his partner and estrangement
from his children.
CASE STUDY 2
A request for HIV testing may indicate anxiety not risk
AIDS anxiety and sexual identity
Michael is a 39-year-old married man who presents for an HIV
antibody test. During discussion, he reports mutual masturbation
with a male acquaintance. Although sexual transmission of HIV is
highly unlikely from this safe sexual encounter, Michael is
convinced that he has AIDS. On examination he is well and the
antibody test comes back negative. In the meantime, Michael now
thinks that he may be gay and needs to talk to someone about it.
The clinician refers him to a counsellor but continues to offer
psychosocial support, as well as HAV and HBV vaccination.
Testing and pregnant women
Why test pregnant women?
The risk of perinatal transmission of HIV and
HBV can be dramatically reduced by a range of
interventions.
The basis for offering pregnant women HIV
testing is the ability to prevent mother-to-child
transmission. Several studies published in the
mid-1990s demonstrated that AZT (zidovudine,
Retrovir
TM
) monotherapy reduced mother-to-
child transmission from 25% to 8%.
2,3,4
The use
of combination therapy plus planned caesarean
delivery and bottle-feeding has reduced HIV
transmission to less than 2%.
5,6,7
Mother-to-child
transmission of HIV has fallen dramatically in
countries where antiretroviral therapy is available
to pregnant women.
8
Interventions to prevent HBV infection are
well established and reference to the National
Health and Medical Research Councils
Immunisation Handbook is advised.
A proven intervention for preventing perinatal
transmission of HCV does not currently exist and
the value of the universal offer of testing is
unclear.
9
There is little risk of transmission via
breast milk unless blood is present.
HIV testing during pregnancy
Pregnancy is a time when women are in contact
with medical clinicians, and it provides an oppor-
tunity for detection of previously undiagnosed
infections.
Australian health policy states that HIV testing
of pregnant women should follow standard guide-
lines in regards to risk assessment, pre-test coun-
selling and informed consent.
10
However, research
shows that many women fail to report risk factors
for HIV until after a positive diagnosis, and there-
fore standard risk assessment may be inadequate to
determine who requires HIV testing.
11
When decid-
ing whether to have an HIV antibody test, all
women should be informed of the substantial ben-
ets of determining HIV status in the prevention of
mother-to-child HIV transmission.
HIV counselling during pregnancy
The issues to be discussed during pre-test coun-
selling listed in Table 8.1 remain relevant for preg-
nant women.
Discussion of the implications of a positive test
result should be extended to include the implica-
tions for the child and, in the case of HIV, should
include discussion of treatment options and ways
of preventing perinatal transmission. US and
Australian guidelines on antiretroviral manage-
ment in HIV-infected, pregnant women may
provide the clinician with a detailed understanding
of treatment, toxicity and mode-of-delivery issues
in these women. To facilitate informed decision-
making by the patient, consideration may be given
to the risks as well as the benets of interventions.
For instance, although combination antiretroviral
therapy is regarded as safe for infant and mother,
there may be an increased risk of rare, life-
threatening side-effects in the mother and birth
abnormalities in the infant. The use of written
information may aid the pre-test counselling
process. Discussion of an equivocal result may also
be considered, given that pregnancy may slightly
increase the likelihood of an indeterminate result.
Post-test counselling of positive tests results
should involve all of the points listed in Table 8.2.
Considerable anxiety and guilt may be associated
with diagnosis during pregnancy. Special atten-
tion should be paid to the psychosocial aspects of
receiving a positive test result during pregnancy.
Counselling should include an assessment of the
negative effects of diagnosis (e.g. discrimination,
domestic violence, psychological difculties) and
should provide information on how to minimise
these. The clinician should evaluate an HIV-
infected pregnant woman to determine her need
for psychological and social services. Specialist
counsellors or midwives with training in this area
may be engaged during this process. The implica-
tions of the test result for both mother and child
should be reiterated, as should treatment options
and measures for preventing perinatal transmis-
sion so the woman can make informed decisions
regarding her options.
US guidelines can be found at
www.aidsinfo.nih.gov
Australian testing guidelines and standards
of care for pregnant women with HIV can
be found at http://www.health.gov.au/hfs/
pubhlth/ancard
The Commonwealth Department of Health
and Ageing has developed guidelines for
HCV testing which can be linked via the
ASHM website at www.ashm.org.au.
Summary
Pre-test and post-test counselling for HIV and
viral hepatitis provides the clinician with the
opportunity to review and reinforce prevention
and risk reduction messages. It also protects human
rights by facilitating the individuals ability to
make an informed decision regarding testing and
helps prepare patients for positive test results. The
benets of early diagnosis, in terms of access to
treatments and improved disease outcomes,
should be highlighted when recommending testing.
In the context of a positive result, post-test coun-
selling deals primarily with psychosocial issues
and early follow-up is recommended.
ASHM can provide information and educa-
tion resources on pre- and post-test counselling.
References
Research. Annual Surveillance Report: HIV/AIDS,
hepatitis C and sexually tranmissible infections in
Australia. Sydney: NCHECR; 2000.
2 Connor EM, Sperling RS, Gelber R, et al. Reduction
of maternal-infant transmission of human
immunodeciency virus type 1 with zidovudine
treatment. N Engl J Med 1994;331:1173-1180.
3 Matheson PB, Abrams EJ, Thomas PA, et al.
Efcacy of antenatal zidovudine in reducing
perinatal transmission of human immunodeciency
virus type 1: the New York City Perinatal HIV
Transmission Collaborative Study Group. J Infect
Dis. 1995;172:353-358.
4 Aleixo LF, Goodenow MM, Sleasman JW, et al.
Zidovudine administered to women infected with
human immunodeciency virus type 1 and to their
neonates reduces pediatric infection independent of
an effect on levels of maternal virus. J Pediatr
1997;130:906-914.
5 The International Perinatal HIV Group. The mode of
delivery and the risk of vertical transmission of
human immunodeciency virus type 1 a meta-
analysis of 15 prospective cohort studies. N Engl J
Med 1999:340(13):977-987.
6 Mandelbrot L, et al. Perinatal HIV-1 transmission,
interaction between zidovudine prophylaxis and
mode of delivery in the French perinatal cohort.
JAMA 1998;280:55-60.
7 Parrazini F for The European Mode of Delivery
Collaboration. Elective caesarean-section versus
vaginal delivery in prevention of vertical HIV-1
transmission: a randomised clinical trial. Lancet
1999;353:1035-1039.
8 Duong T, et al. Vertical transmission rates for HIV in
the British Isles: estimates based on surveillance
data. BMJ 1999;319:1227-1229.
9 Gibb D, et al. Mother-to-child transmission of
hepatitis C virus: evidence for preventable
peripartum transmission. Lancet 2000;356:904-907.
10 ANCARD/IGCARD. HIV testing policy. Canberra:
Commonwealth Department of Health and Aged
Care, 1998.
11 Barbacci MB, et al. Human immunodeciency virus
infection in women attending an inner-city prenatal
clinic: ineffectiveness of targeted screening. Sex
Trans Dis 1990;17:122-126.
Introduction
The course of HIV infection has been altered sig-
nicantly by the use of potent antiretroviral therapy
and treatments for HIV-related opportunistic ill-
nesses in developed countries. In the era of combi-
nation antiretroviral therapy, many HIV-infected
patients remain well ten years after their first
AIDS-related illness. Nevertheless, HIV disease
management remains a complex and evolving
area of medicine which is constantly reshaped as
new, scientic evidence emerges.
This chapter aims to provide the HIV non-spe-
cialist clinician with an update on the management
of HIV disease and to describe the role of the pri-
mary care clinician in the shared management of
HIV-infected patients. When managing patients
with HIV disease, the primary care clinician often
works in conjunction with a clinician, either a gen-
eral practitioner or physician, who is able to pre-
scribe antiretroviral drugs under Section 100 of the
Pharmaceutical Benets Scheme (PBS), as well as
other services and agencies.
The challenges of managing patients
with HIV infection
Management of HIV as a chronic disease
There are many challenges in the management of
HIV-infected patients, some of which are com-
mon to the management of other chronic condi-
tions. For example, the patient needs to be
informed about the nature of the disease and
potential treatments. Assistance in adherence to
medication is particularly relevant in the manage-
ment of HIV disease given the potential for drug
resistance if doses are missed. The clinician also
has a role in exploring a range of psychosocial
and sexuality issues, and in encouraging a sense of
hope through discussion of treatment options.
Management of HIV infection as a chronic dis-
ease is shaped by the stigmatisation attached to
HIV/AIDS and the fear or anxiety patients may
exhibit following diagnosis.
The quality of the doctor-patient relationship
is central to the successful long-term management
9
Primary care management of HIV disease
David Orth General Practitioner and Sexual Health Clinician, Brunswick Street Medical Centre,
Brisbane, Queensland.
Jennifer Hoy Infectious Diseases Physician, Alfred Hospital, Melbourne, Victoria.
Warren Fitzgerald HIV Services Manager, Queensland AIDS Council (QuAC), South Brisbane, Queensland.
John Patten Sexual Health Physician, Sexual Health & AIDS Service, Prince Charles Hospital Health
Service District, Queensland.
Anthony Allworth Infectious Diseases Physician, Royal Brisbane Hospital, Queensland.
Key points
HIV infection remains a complex disease and its management
continues to evolve.
The period of assessment and management of people living
with HIV/AIDS after diagnosis and before anti-HIV treatment is
active for both patient and doctor. The role of the primary care
clinician during this time is one of support, education,
monitoring and referral.
Knowledge of the conditions and illnesses associated with the
stages of HIV immunodeciency is necessary in the clinical
monitoring of HIV-infected patients. Signs and symptoms of
HIV disease are discussed in Chapter 6.
Combination antiretroviral therapy is available for the treatment
of HIV/AIDS. Long-term suppression of HIV replication occurs
in approximately 60% of people who commence triple
combination therapy. Viral suppression produces strong
immune recovery in most patients. Specialists and general
practitioners who have completed HIV prescriber courses may
prescribe antiretroviral therapy through Section 100 of the
Pharmaceutical Benets Scheme (PBS).
The primary care clinician has a role in supporting adherence
with patients who are taking antiretroviral therapy, as well as
monitoring for adverse events and drug interactions.
A focus on general health maintenance, psychosocial issues
and support remains central to the care of HIV-infected patients
in the era of combination antiretroviral therapy.
of HIV. Nurturing this long-term therapeutic rela-
tionship is a major task for the primary care clini-
cian. The key characteristics of this relationship
are honesty, accessibility, a demonstrated commit-
ment to confidentiality and the privacy of the
patient, and medical expertise. Offering frequent
and/or long consultations may be appropriate and
provision of an after-hours contact number may
be considered. The therapeutic relationship may
be enhanced if the clinician demonstrates that
he/she is comfortable with HIV-infected patients
(e.g. by taking blood) and gay or bisexual patients
(e.g. by openly discussing sexual matters).
The goals of the therapeutic relationship specif-
ically in relation to patients with HIV include:
maintenance of an effective, collaborative,
therapeutic relationship;
thorough, ongoing assessment;
education of the patient with regard to HIV
infection, natural history, transmission and the
effects of therapy;
provision of information and referral
regarding medical and psychosocial resources
and services;
facilitation of effective medical intervention to
maximise the patients health prior to and
during treatment.
Natural history and treatments
Following acute infection with HIV (Chapter 4),
there is a stage of clinical stability where immuno-
logical and virological markers remain relatively
stable. During this period, homeostasis exists
between the amount of HIV produced and cleared
each day, and the number of CD4 cells produced
and destroyed each day. Subsequently, clinical sta-
bility may continue despite deterioration in labora-
tory markers as the immune system fails to control
the amount of HIV produced (Chapter 1). At this
time, the amount of HIV measurable in plasma
(the viral load) may increase as the number of
CD4 T-lymphocytes falls. Average time to AIDS is
about ten years but progression rates vary widely
at the individual level. Determinants of the rate of
disease progression include age and virological
and host factors.
Constitutional symptoms (lethargy, fatigue,
diarrhoea, weight loss and night sweats) may
occur in the presence of a high viral load at any
stage of disease. Early symptoms of immune de-
ciency begin to appear when the CD4 count falls
below normal levels (Figures 1.1 and 6.1). As the
CD4 count decreases to levels below 200 cells/l,
the patient is at greater risk of several opportunis-
tic infections.
An understanding of the natural history of
HIV disease provides the basis for treatment deci-
sions. Experts generally recommend commence-
ment of therapy as surrogate markers deteriorate
prior to onset of symptomatic disease, certainly
prior to severe immune deciency. However, the
best time to commence antiretroviral therapy is
yet to be established. See HIV treatment issues
on page 78 for further details.
Assessment and monitoring
Assessment and monitoring of the HIV-infected
patient relates to general physical health, psy-
chosocial wellbeing, as well as immune and viro-
logical status.
TABLE 9.1 Checklist: Initial assessment of
the HIV-infected patient
General assessment including medical history, family history,
drug and alcohol history, smoking history
Full psychosocial assessment
Targeted physical examination including weight, cardiovascular
status, oral and dental health, skin and general systems
examination
Sexual health review and a pelvic/anogenital examination
Screens for infections such as toxoplasmosis (Toxoplasma
IgG), tuberculosis (Mantoux test and chest X-ray),
cytomegalovirus (CMV IgG), syphilis, and hepatitis B and A
(HAV IgG, HBsAg, anti-HBs, anti-HBc)
Screen for hepatitis C (anti-HCV, HCV PCR) for patient with risk
factors and a CD4 <350 cells/l
Blood tests, including HIV RNA viral load, CD4 count, CD4
percentages, fasting cholesterol, triglycerides and glucose,
liver function tests, serum amylase, creatinine phosphokinase,
urea and electrolytes and a full blood count (FBC)
HIV resistance genotyping (can be conducted in consultation
with an HIV-experienced clinician)
Vaccination history needs to be noted and future vaccinations
discussed. The patient should be offered HBV and HAV
vaccination in the absence of established immunity or
infection. Live vaccination should not be given to HIV-infected
patients. Both Fluvax and Pneumovax are recommended as
per NHMRC guidelines.
1
9 Primary care management of HIV disease
Data from the Multicenter AIDS Cohort Study
(MACS) of HIV-infected men conrmed that both
the CD4 count and HIV viral load are prognostic
markers of likely disease progression and clinical
illness in HIV disease. As can be seen from Table
9.2, the proportion of men who progressed to an
AIDS-dening illness was greatest for those with
the highest viral loads and lowest CD4 cell counts.
Within each stratum of CD4 cell count, prognosis
was best for those with the lowest viral load.
CD4 cell count
In untreated HIV infection, progressive immune
damage will occur, expressed as a loss of CD4
cells at an average rate of 60-80 cells/l per year.
Some patients may have a more rapid course,
while others will remain stable for longer.
There are levels of immune deciency that are
associated with greater risk of HIV-related condi-
tions and opportunistic illnesses (Figure 1.1). For
example, when the CD4 cell count falls to between
200 and 500 cells/l, oral hairy leukoplakia, skin
conditions such as seborrhoeic dermatitis and pso-
riasis, recurrent varicella-zoster virus infection
(shingles), and bacterial pneumonia may occur.
CD4 cell counts below 200 cells/l are associated
with an increased risk of Pneumocystis carinii
pneumonia (PCP), cerebral toxoplasmosis, candidi-
asis, Kaposis sarcoma and cryptococcosis.
Advanced immunodeciency occurs at CD4 cell
counts below 50 cells/l, at which stage the individ-
ual is at risk of cytomegalovirus (CMV) retinitis,
disseminated mycobacterium avium complex
(MAC) infection, cryptosporidiosis and micro-
sporidiosis, primary central nervous system lym-
phoma and HIV-associated dementia, and non-
Hodgkins lymphoma. Opportunistic infections are
discussed in greater detail in Chapter 6.
The CD4 cell count is calculated by the per-
centage of CD4 cells in the lymphocyte compo-
nent of the white cell count. The total number of
CD4 cells will vary according to the white cell
count and lymphocyte count. It is important to
assess changes in the total CD4 cell count in the
context of the percentage of CD4 cells and vari-
ability of the lymphocyte number secondary to
intercurrent illnesses. A single measurement may
be misleading because factors such as intercurrent
infection, vaccination, menstrual cycle, and the
time of day blood is taken can impact on results.
Consequently, evaluation should focus on the
trend in CD4 cell levels rather than a single result.
A number of tests need to be performed over a
Initial assessment
During initial consultations with an HIV-infected
patient, a comprehensive medical and psychoso-
cial assessment should be conducted. General dis-
cussion concerning the impact of HIV/AIDS on
the patient, issues of sexuality and social support
will build rapport and facilitate appropriate man-
agement and referral. The patients priorities with
regard to HIV disease and his/her knowledge of
HIV/AIDS need to be established prior to discus-
sion of treatment options and transmission pre-
vention. Ascertaining whether or not the patient
sees an HIV specialist and whether a referral is
sought may shape the consultation.
Initial medical assessment concerns establish-
ing the stage of HIV disease and assessment of co-
morbidities. A comprehensive range of blood
tests, serological tests and clinical examination
should be conducted (Table 9.1).
Chapter 8 addresses how to deliver a positive
HIV result to a patient and conduct early follow-
up. In the context of HIV diagnosis, the initial
assessment may take place over several weeks or
months and psychosocial issues may take priority
for the patient at this time.
Coinfection with viral hepatitis
Chronic liver disease commonly affects people
with HIV infection and screening for viral hepati-
tis is recommended. Coinfection with either HBV
or HCV is associated with greater risk of chronic
liver disease and cirrhosis, and may affect
survival. Viral hepatitis coinfections can impact
on antiretroviral regimen choices as well as other
lifestyle and health issues. The avoidance of alco-
hol and other potential hepatotoxins is important,
as is the prevention of other hepatic infections.
Vaccination against hepatitis A and hepatitis B is
recommended for those who are not immune
(Chapters 1, 5 and 10).
Markers of HIV disease: immunological
and virological status
Immunological and virological status is evaluated
by a general physical examination, T-cell subsets
and viral load testing every three months. The
CD4 cell count is the main measure of immune
damage in HIV-infected people. The HIV RNA
viral load (the number of viral copies per millilitre
of blood plasma) is the key virological assay. In
the absence of treatment, higher viral load is asso-
ciated with faster CD4 cell decline and the devel-
opment of AIDS-related conditions.
Viral load is used to assist in making the decision to
initiate antiretroviral therapy (along with the pres-
ence or absence of symptoms and the levels of CD4
cells), to monitor the response to antiretroviral
therapy and to identify treatment failure.
Monitoring HIV infection
The Australian National Council on AIDS,
Hepatitis C and Related Diseases (ANCAHRD)
has produced a document: Model of Care for
HIV Infection in Adults, which sets out the
recommended schedule of monitoring for HIV
infected adults, both treated and untreated. It is
available for downloading at www.ashm.org.au.
Patients will require more regular reviews if they
are more immunosuppressed or receiving anti-
retroviral therapy.
In general, the untreated, immunocompetent
patient (CD4 cells >350/l) should be reviewed
every 36 months, while the patient with less than
350 CD4 cells/l or receiving antiretroviral therapy
needs review every 23 months.
5
Graphs and sum-
mary pages contained in the Model of Care are
essential tools to assist the clinician and the patient
in monitoring changes in viral load and immune
function, as well as general health maintenance.
Psychosocial assessment
Effective management of HIV-infected individuals
involves an approach which addresses psychoso-
cial as well as biomedical factors. In addition to
psychosocial issues related directly to HIV infec-
tion, the social stigma and marginalisation experi-
enced by groups most affected by HIV may com-
pound the psychological, social and emotional
impact of HIV infection. The cumulative grief
experienced by many HIV-positive people who
have lost close friends to HIV should be considered
when conducting psychosocial assessment. Social,
emotional and educational support is available
through AIDS Councils and HIV-positive peoples
groups in each State and Territory (Chapter 14).
Psychosocial assessment and management
involves consideration of the following issues:
self-esteem and body image;
stigmatisation and discrimination;
family and social relationships/supports;
sexual relationships and related issues of dis-
closure and safe sex;
depression and emotional issues (e.g. anger,
denial, anxiety);
drug and alcohol use;
TABLE 9.2 Surrogate markers and risk of progression
to AIDS
CD4 cell count Viral load % AIDS progression in men
copies/ml over 3 years over 9 years
<200/l <10,000 14% 64%
10,000 30,000 50% 90%
>30,000 86% 100%
200-350/l 10,000 7% 66%
10,000 30,000 36% 85%
>30,000 64% 93%
>350/l <10,000 7% 54%
10,000 30,000 15% 74%
>30,000 40% 85%
Adapted from Multicenter AIDS Cohort Study
1,2
period of time to provide an accurate picture of
the patients immune function. These test results
enable the clinician to form an assessment of the
course of an individuals HIV disease and the rate
of disease progression.
Viral load
Plasma viral load estimates provide the strongest
long-term prognostic information for HIV patients.
The plasma viral load is a measure of the balance
between the amount of HIV produced each day and
the amount of HIV cleared by the immune system.
Viral load (the amount of HIV RNA in the
plasma) can be measured by two different tech-
nologies branched chain DNA (bDNA) or reverse
transcriptase polymerase chain reaction (RT PCR).
The two commercially available methods have a
strong correlation at the population level but
results may differ by up to 1 log in an individual, so
it is not recommended that the two assays are used
interchangeably in a single individual.
The laboratory will give results in both log
number of copies/ml and absolute number of
copies/ml. A signicant change in viral load is an
increase or decrease of greater than 0.5 log.
Changes of less than 0.3 log are considered to be
within the variability of the laboratory test perfor-
mance (Table 9.3 and Case Study 1). The lower
limit of detection of the assays is currently at
4050 copies/ml, and viral loads below this level
are reported as undetectable; however this does
not mean that there is no HIV present.
4
issues around pregnancy and motherhood for
women;
compliance with drug therapy and related
lifestyle issues;
nancial/employment situation;
health care satisfaction.
Most of these evaluations will take a number of
consultations to complete and ongoing assess-
ment is recommended.
Key relationships and support systems are
pivotal to the wellbeing of the patient. One of the
most important support systems for many people
is their biological family, therefore assessment of
family relationships and social support should be
conducted. Issues to consider include whether the
family is aware of the patients sexuality and/or
HIV status, their reaction to this information
and/or the patients reasons for not telling them.
Friends may also provide an invaluable support
network.
Other questions to ask are: is the patient in a
relationship and what is the quality of that rela-
tionship? Does the partner know of the
persons HIV status? How does the persons HIV
status affect the relationship sexually or emotion-
ally? Patients who lack supportive and trusting
relationships may be isolated and vulnerable, and
referral to community organisations or other ser-
vices may be appropriate (Chapter 14).
Use of drugs and alcohol should be explored
in a non-judgemental way. Substance abuse may
be a form of self-medication for depression or
may perpetuate denial and avoidant behaviours.
Referral may be made to a treatment program or
other specialist service. An accurate drug and
alcohol assessment is essential prior to com-
mencement of antiretroviral therapy due to the
possibility of serious and life-threatening drug
interactions.
For HIV-infected women, issues of family and
children may be of particular concern. Fears
about transmission or future care may inuence a
womans desire for children, and full education
and discussion is advised (Chapter 8). For a
woman who already has children, there may be
concerns that her children are HIV-infected. Most
CASE STUDY 1
When is a viral load change signicant?
Viral load changes and adherence
Alex has regular monitoring of his viral load and CD4 cell count
every six months. When his viral load reaches 48,990 copies/ml
(4.69 log) and his CD4 cell count is 300 cells/l, he commences
combination antiretroviral therapy.
He has a good virological response to treatment, recording a
viral load of 570 copies/ml (2.76 log) three months later. Over the
rst 12 months of therapy his viral load is measured at 800 and
1,000 copies/ml (2.90 and 3.00 log). No action is taken by the
clinician, as these results are not signicantly different from the
nadir of 570 copies/ml (i.e. not greater than a 0.3 log difference
from 2.76 log).
However, 18 months later his viral load is 6,500 copies/ml
(3.81 log). This is a signicant rise in viral load (>0.5 log), which
prompts a discussion of his adherence to therapy and whether he
has taken any new medication that may have interacted with his
antiretroviral drugs. Alex says that he nds it difcult to remember
to take his pills and admits missing doses.
The clinician explores strategies to assist Alex in taking his
pills, such as keeping pills in highly visible locations (e.g. next to
his bed, toothbrush or keys) or using a beeper.
TABLE 9.3 Signicance of viral load changes
Biologically relevant changes in viral load (>0.5 log) and changes considered within the variability of the laboratory
assay (>0.3 log)
Copy Log
10
Log
10
Fold Signicant
number change from change change from
10,000 copies/ml 10,000 copies/ml
5,000 3.7 -0.3 0.5 No
10,000 4.0 0 1.0
20,000 4.3 +0.3 2.0 No
50,000 4.7 +0.7 5.0 Yes
100,000 5.0 +1.0 10 Yes
infants with HIV develop signs of immune de-
ciency within the rst year of life and antiretrovi-
ral therapies are available to children, although
adherence to therapy can present difculties. For
HIV-infected women requiring support, referral
to Positive Womens groups is recommended
(Chapter 14).
In the era of combination antiretroviral therapy,
patients may wish to address issues of returning to
work, education or relationships in light of their
improved prognosis. The demands of long-term
adherence to therapy or the physical manifesta-
tions of drug toxicities may also give rise to other
psychosocial concerns regarding body image,
lifestyle and/or sexuality.
Psychological assessment
6
Several Australian studies indicate a high preva-
lence of major depressive symptoms and dys-
thymia among HIV-infected people,
7,8,9
with par-
ticularly high rates among patients with fewer
social supports and lower income. Depressive
symptoms may impact on the individuals ability
to maintain safe sexual practice or lead to suicidal
ideation.
Psychological assessment should be conducted
to identify and treat major psychiatric illness.
Recent acquisition of HIV may indicate that the
patient has participated in some sort of self-
destructive behaviour, which may be related to
depression or suicidal ideation, drug and alcohol
dependence, post-traumatic stress disorder or a
range of other problems. Depression in HIV-
infected people may be inuenced by factors such
as social rejection, progression of HIV disease,
lack of support networks or alcohol and drug use,
and these factors should be identified and
addressed.
Patients with signicant immunosuppression
may be at risk of developing organic brain disease
and consideration should be give to the mental
health implications of immune status. In addition,
depressive, neuropsychological side-effects may be
caused by antiretroviral agents, most commonly
efavirenz.
Health promotion
Prevention
It is important that HIV-infected people have a
clear understanding of HIV transmission so that
they do not pass on the infection (Chapters 2 and
3, Appendix 1). A patients knowledge of trans-
mission, especially with regard to his/her own
(possibly changing) behaviour, needs to be
broached at regular intervals over the course of
the therapeutic relationship. The risk of HIV
transmission when the patient has undetectable or
low viral load must also be addressed. Although
viral load in the blood plasma often correlates
with viral load in semen and vaginal uids, this is
not necessarily the case. Consequently, a person
with undetectable virus in the blood may still be
able to transmit HIV. The benets of safe behav-
iours to the patient may be reiterated, such as pre-
vention of sexually transmitted infections.
Unprotected sex between HIV-infected individu-
als may carry the risk of re-infection with a drug-
resistant or more aggressive virus, which may
accelerate disease progression.
Post-exposure prophylaxis (PEP)
In cases of exposure (e.g. through condom break-
age), PEP may help patients prevent transmission
of HIV to their partners. As described in detail in
Chapter 4, PEP involves taking antiretroviral
medication within 72 hours of a high-risk expo-
sure to HIV. Knowledge of this intervention can
help to increase the condence of HIV-infected
people to be sexually active, particularly those in
serodiscordant relationships, but must not be pro-
moted as a stand-alone prevention strategy.
National guidelines, on the use of PEP for non-
occupational exposure have been produced see
Chapter 4 for details.
Education
The clinician may need to provide the patient with
information about HIV disease, monitoring and
treatment to facilitate patient participation in
health and treatment decisions. Appendix 1 pro-
vides a summary of basic information about HIV
infection, which may assist the clinician in educat-
ing the patient. As concepts are introduced and
reviewed, many patients will come to a highly
sophisticated understanding of their situation.
The clinician has a central role in interpreting
test results and providing the patient with an
understanding of his/her prognosis. The patient
should be aware that CD4 cell counts and viral
load can vary from test to test and that trends are
more important than absolute numbers.
Graphing results over time may be a helpful way
of demonstrating the patients position. While
population-based studies have provided an
overview of average rates of disease progression,
the patient should know that there is no way
of predicting the course of HIV disease in individu-
als. Patient education involves conveying the
uncertainties of HIV disease, such as time to dis-
ease progression and response to therapy.
Patient education also involves provision of gen-
eral dietary and lifestyle advice. A healthy, bal-
anced diet (Chapter 10), low levels of stress and
regular exercise are recommended. Potential
drug-related harms and drug interactions with
antiretroviral therapy should be discussed.
TABLE 9.4 Assessment and monitoring of the HIV-infected patient
Three-monthly reviews in all HIV-infected patients:
Collection of history and symptom review
General physical monitoring
Weight, blood pressure, oral and dental checks
Full blood count
Liver function tests and amylase
CD4 cells and percentage
Viral load
Psychosocial assessment and support
Patient education (transmission prevention and
treatment updates)
Health promotion (alcohol avoidance for HCV
co-infected patients, smoking cessation, dietary
adjustment)
Six-monthly reviews in all HIV-infected patients:
Ophthalmological assessment if CD4 cell count is
below 50 cells/ml (rule out asymptomatic CMV retinitis)
Pap smears in women with previous evidence of
cervical dysplasia. Anal smears are performed by
some GPs but predictive value of subsequent anal
carcinoma is unproven.
Annual reviews for all HIV-infected patients:
Assessment of immunity to hepatitis B
Vaccinations
Cervical cytology by Pap smear in women
Additional monitoring for patients taking antiretroviral
therapy
Treatment-related monitoring is primarily conducted by
the antiretroviral prescriber
Frequent review during the rst month of treatment:
Monitoring for severe side-effects (e.g.hypersensitivity,
Stevens-Johnson syndrome, CNS toxicity)
Management of treatable side-effects (e.g. nausea,
diarrhoea)
Adherence monitoring and support. Tips to maximise
adherence. Consideration of change of medication.
Referral.
Three-monthly reviews:
Assessment of potentially adverse effects of treatment
(e.g. peripheral neuropathy, lipoatrophy, lipodystrophy)
Ongoing adherence monitoring and support
Six-monthly reviews:
Fasting cholesterol (including HDL and LDL),
triglycerides, insulin and oral glucose tolerance
Monitoring of serum lactate, particularly in
symptomatic patients, to detect lactic acidemia related
to nucleoside analogue therapy (the utility of this
monitoring remains unclear)
Annual reviews:
Physical assessment for lipodystrophy, including DEXA
scan for assessment of fat and bone mineral density
Assessment of cardiovascular risk factors (family
history, smoking, hypertension, hyperlipidemia, insulin
resistance)
Resources for health care professionals
and positive people
There is a wide range of resources available to
support clinicians and patients. ASHM distributes
regular bulletins to members and has a website
providing information for clinicians and patients
which is regularly updated. Treatment informa-
tion for patients is also available from community
organisations (Chapter 14).
HIV treatment issues
The aim of antiretroviral therapy is to reduce HIV
viral load, prevent HIV disease progression and
produce immunological reconstitution. The pri-
mary marker of successful therapy is suppression
of HIV viral load to undetectable levels.
The effect of potent combination therapy on
immune function, survival, AIDS progression and
hospitalisation has been dramatic.
10
The relation-
ship between viral load and treatment benefit
from antiretroviral therapy has been analysed in
over 5,000 patients enrolled in 18 clinical trials.
These studies have shown that:
11
reduction in viral load is associated with
improved outcome, with each 1 log (10-fold)
reduction reducing the risk of clinical progres-
sion by 65%;
reduction in risk of disease progression or
death is independent of baseline plasma HIV-1
RNA and CD4 cell count;
benet is independent of the increase in CD4
cell counts secondary to treatment;
rates of mortality, illness and hospitalisation
have fallen signicantly.
The treatment-induced reduction in viral load is
determined by several factors, including the
potency of the regimen. Viral load reductions of
greater than 2.0 log are expected with rst-line
combination antiretroviral therapy regimens.
Viral load reductions are always greater in treat-
ment-naive individuals.
Initiating antiretroviral therapy
The decision to commence antiretroviral therapy
is made on the basis of the risk/benet analysis
and the patients readiness to take treatment.
Antiretroviral treatment guidelines, based on
expert opinion and available scientic evidence,
have been developed in Australia and overseas to
guide decisions about commencing and switching
treatment.
12,13
Recommendations prior to 2001, were based on
the amount of virus present (>10,000 copies/ml) or
an abnormal CD4 cell count (<500 cells/l).
14
However, the increased recognition of the risks of
antiretroviral therapy in the form of long-term
metabolic toxicities, combined with the realisa-
tion that eradication of HIV is unlikely to occur,
has resulted in recommendations to delay the ini-
tiation of antiretroviral therapy until the CD4 cell
count is around 350 cells/l.
The following are indications to begin treat-
ment with combination antiretroviral therapy:
symptomatic HIV infection;
asymptomatic HIV infection with a CD4 cell
count below 350 cells/l.
The question of when to commence antiretroviral
therapy remains a topic of debate among expert
physicians and GPs. Some may recommend therapy
for a patient with a CD4 cell count greater than
350 cells/l and a viral load greater than 30,000
copies/ml by bDNA (or greater than 55,000
copies/ml by RT-PCR).
Deferral is generally recommended if a patients
CD4 cell count is greater than 350/l and viral
load is lower than 30,000 copies/ml bDNA (or
55,000 copies/ml by RT-PCR).
The nal decision rests with the patient and
clinician in consultation. In making the decision
to treat, consideration must be given to the
patients commitment to therapy, his/her aware-
ness of the importance of strict adherence to the
regimen, and the potential for adverse effects.
Advice regarding the decision can be obtained
from the antiretroviral prescriber and a number of
sources listed in Chapter 14.
Treatment regimens
There are three classes of approved antiretroviral
medications: nucleoside analogue reverse tran-
scriptase inhibitors (NRTIs); non-nucleoside
reverse transcriptase inhibitors (NNRTIs) and
protease inhibitors (PIs). These antiretroviral drugs
inhibit one of two viral enzymes reverse tran-
scriptase or protease. Anti-HIV medications and
their side-effects are summarised in Table 9.5.
Patients commencing treatment should be
started on a combination of either three or four
drugs. Generally, a combination includes drugs
from at least two different drug classes. In general,
patients initiate treatment either with two nucleo-
side analogues and an NNRTI, or two nucleoside
analogues and a PI. Treatment regimens are
developed at the individual level based on dosing
requirements, toxicity proles and co-morbidities.
Assessment of response to therapy
For a patient on treatment, a signicant increase
in HIV RNA or failure to achieve undetectable
viral load requires consideration of the following
factors:
The patient may show poor adherence and
changes to the treatment regimen may be
required.
Drug levels may be too low to suppress HIV
replication due to drug interactions or poor
absorption, requiring dose adjustments or a
change in regimen.
Resistance to the antiretroviral drugs may have
developed and resistance assays may be con-
ducted by the antiretroviral prescriber.
These tests must be interpreted in the context of
the patients antiretroviral history.
Side-effects and interactions
Side-effects of antiretroviral therapy may be early
or start up (e.g. headache), persistent (e.g. diar-
rhoea) or long term (e.g. lipodystrophy).
15
Each
antiretroviral drug has its own particular side-
effect prole with which the primary care clini-
cian should be familiar (Table 9.5).
The patient should be supported through ini-
tial side-effects, most of which are very common
and usually short-term (www.medscape.
com/Medscape/HIV/Treatmentsupdate). Some
side-effects are life-threatening and necessitate
immediate cessation of the medication. These
include acute hepatitis, severe rashes including the
Stevens-Johnson syndrome (associated with the
NNRTIs) and the abacavir hypersensitivity reac-
tion.
This reaction occurs within six weeks of start-
ing abacavir and symptoms include fever, nausea,
vomiting, diarrhoea and malaise, with or without
rash. Lactic acidosis is a rare adverse event associ-
ated with the nucleoside analogues, which may
lead to organ failure and death. Usually the anti-
retroviral prescriber will be monitoring the
patient very closely through this phase. If the
patient presents to the primary care clinician with
a problem, the antiretroviral prescriber should be
directly consulted.
Protease inhibitors and nucleoside analogues
have been associated with the lipodystrophy syn-
drome, which develops as a long-term toxicity of
antiretroviral therapy. Lipodystrophy syndrome
involves:
fat gain (particularly visceral abdominal fat);
peripheral subcutaneous fat loss in arms, legs,
buttocks, face;
increased serum lipids and insulin resistance.
Chapter 6 includes a photograph of the clinical
presentation of lipodystrophy. The mechanism
underlying this syndrome and its treatment is cur-
rently under investigation.
16
It is important to recognise a potential
increased cardiovascular risk in patients with the
development of insulin resistance and hyperlipi-
daemia. Appropriate management and attention
to other risk factors such as hypertension and
smoking is required.
Drug interactions
The potential for drug interactions should also be
considered. The PIs and the NNRTIs are
metabolised by the hepatic cytochrome P450 3A4
enzymes. The PIs inhibit the P450 3A4 enzymes
with varying potency and the NNRTIs can induce
or inhibit the enzymes. It is no longer possible to
remember all the drug interactions and there are
several sources regularly updated that outline pre-
dicted interactions and known interactions. These
can be found at the following websites:
www.hiv-druginteractions.org and
www.georgetown.edu/departments/
pharmacology/davetab.html.
Always check these websites before introducing
any new drugs. It is also known that some com-
plementary medicines can cause reductions in PI
concentrations (e.g. St Johns Wort, garlic pills).
The recreational drug ecstasy may also interact
with PIs to produce very high levels of ecstasy in
the blood and extreme caution should be advised
regarding use of ecstasy by people taking PIs.
Drugs contraindicated with concomitant use
of PIs and delavirdine because of potential life-
threatening reactions are:
terfenadine, astemizole non-sedating antihist-
amines (use loratidine as an alternative);
cisapride prolongation of the Q-T interval,
torsade de pointes arrhythmias;
lovastatin rhabdomyolysis;
midazolam, triazolam prolonged sedation.
(It is important to inform anaesthetists about
antiretroviral therapy because of the impact on
procedures such as endoscopy or bron-
choscopy. Propofol is recommended as an
alternative.)
Additional contraindications and cautions apply
in the case of the protease inhibitor ritonavir.
TABLE 9.5 Antiretroviral medications
Nucleoside/nucleotide analogue reverse transcriptase inhibitors*
Nucleoside analogue Dose (adults) Adverse effects
abacavir 300 mg bd Hypersensitivity reaction (potentially lethal if rechallenged),
headache, malaise, GI intolerance
Combivir (AZT/3TC) 300mg/150mg bd See AZT and 3TC above
didanosine (ddI) 400 mg daily GI intolerance, diarrhoea, taste disturbance,pancreatitis,
peripheral neuropathy
dideoxycytidine (ddC) 0.75 mg tds Stomatitis, oropharangeal ulceration, pancreatitis,
peripheral neuropathy
lamivudine (3TC) 150 mg bd Headache, nausea, diarrhoea
stavudine (d4T) 40 mg bd Headache, GI intolerance, peripheral neuropathy,
pancreatitis
tenofovir 300mg daily Headache, GI intolerance, rare renal toxicity
Trizivir (abacavir, AZT/3TC) 300mg/300mg/150mg bd See AZT, 3TC and abacavir above
zidovudine (ZDV, AZT) 250 mg bd GI intolerance, malaise, headaches, macrocytosis
bone marrow suppression, anaemia, myopathy
All nucleoside analogues have the potential to cause mitochondrial toxicity and a syndrome of chronic, low-grade lactic acidemia.
In a small minority of individuals this may progress to life-threatening lactic acidosis.
Non-nucleoside reverse transcriptase inhibitors (NNRTIs)*
NNRTI Dose (adults) Adverse effects
efavirenz 600 mg qd Rash, insomnia, somnolence, psychiatric disturbances,
vivid dreams/nightmares, abnormal liver function tests,
hyperlipidemia
nevirapine 200 mg bd Rash, Stevens-Johnson syndrome, hepatitis
delavirdine 600 mg tds Rash, headaches, abnormal liver function tests
Protease inhibitors (PIs)*
Protease inhibitor Dose (adults) Adverse effects
amprenavir (APV) 1,200 mg bd or 600 mg GI intolerance, rash, headache
with 100 mg RTV bd
atazanavir (ATZ) 400 mg daily or 300 mg/ Elevated bilirubin, jaundice, nausea
100mg daily with RTV
indinavir (IDV) 800 mg td (fasting) Elevated bilirubin, GI intolerance, nephrolithiasis,
or 800 mg bd ingrown toenails, dry skin, mouth and eyes,
with RTV 100 mg bd hair loss, diabetes, hepatitis
lopinavir/ritonavir (LPV) 400 mg/100 mg bd GI intolerance, abnormal liver function, tests
nelnavir (NFV) 1,250 mg bd Diarrhoea, GI intolerance.
ritonavir (RTV) 100-200 mg bd as a GI intolerance, diarrhoea, hepatitis, abnormal liver function
pharmacokinetic tests,
enhancer of
other ARV agents
saquinavir (SQV) 1,200 mg tds or 1600 mg GI intolerance, diarrhoea, headache
with 100 mg RTV once daily
* Drug information current at March 2004. See ASHM website www.ashm.org.au for updated information.
Compliance issues
Medication must be taken properly to be effective
in the long term. If the patient is regularly missing
doses, not following dosing recommendations or
has commenced a new medication/complemen-
tary medicine which affects the metabolism of the
drugs, the reduced concentration of drug allows
for the selection of drug-resistant HIV and fail-
ure of the antiretroviral regimen.
17
Unfortunately,
there is often signicant cross-resistance within
the same class of antiretroviral drugs
18
and resis-
tance to one drug may undermine response to
subsequent regimens. If the patient reports poor
adherence, discussion with the HIV prescriber
may be appropriate to consider simplication of
the antiretroviral regimen to a once- or twice-daily
regimen to make adherence easier. Management of
side-effects may also improve adherence.
In consultation with the patients antiretrovi-
ral prescriber, consider referring the patient for
adherence counselling. The AIDS Councils, spe-
cialist HIV units and domicillary nursing organi-
sations conduct adherence counselling.
Immune-based therapies
Immunomodulators are another form of therapy
for HIV infection currently under investigation.
Subcutaneous interleukin-2 is known to induce
signicant rises in CD4 cells, but treatment cycles
are associated with often incapacitating, short-
term side-effects.
19
The current trials are investi-
gating whether this rise in CD4 cells translates to
a clinical benet in terms of improved survival
and reductions in disease progression to AIDS-
dening illnesses. Other approaches to immuno-
modulation under investigation include therapeu-
tic HIV vaccination.
Prophylaxis
When the CD4 cell count falls below 200 cells/l,
there is an increased risk of opportunistic infec-
tions and prophylaxis may be recommended to
prevent some common opportunistic infections.
Table 9.6 contains the prophylactic regimen of
choice and an alternative prophylactic regimen in
the event of intolerance or drug allergy, and the
CD4 cell count at which prophylaxis is recommen-
ded.
20
For patients who have instituted prophyl-
axis and then experience immune reconstitution,
prophylaxis may be discontinued safely if the
CD4 cell count remains above 200 cells/l for at
least six months. However, prophylaxis should be
recommenced if the CD4 cell count falls below
that mark.
AIDS-related illness
Symptoms in the HIV-infected patient should be
interpreted in the context of the patients current
and past immune function, current therapy and
recent changes in medication or complementary
therapy. In patients with normal CD4 cell levels,
symptoms may represent community-acquired
infections or medication side-effects.
Patients who initiate therapy at low CD4 cell
counts (less than 100200 cells/l) may present
with immune reconstitution illness. Fever, lym-
phadenitis, sweats and fatigue may be related to
localisation of Mycobacterium organisms to the
lymph nodes by a reconstituted immune system.
Other common forms of immune reconstitution
illness are discussed in Chapter 6.
In immunocompromised patients (CD4 cell
count less than 200250 cells/l), certain symp-
TABLE 9.6 Recommended prophylaxis during HIV infection
Opportunistic infection First-line prophylaxis Alternative CD4 cell count
Pneumocystis carinii pneumonia cotrimoxazole dapsone 200 cells/l
1 tab qd nebulised pentamidine
Toxoplasmosis cotrimoxazole 1 tab qd dapsone/pyrimethamine 200 cells/l
Mycobacterium avium complex azithromycin 1,200 mg weekly rifabutin 300 mg qd 50 cells/l
CMV retinitis ophthalmological review 6 monthly 50 cells/l
Pneumococcal pneumonia Pneumococcal vaccine 500 cells/l
inuenza inuenza vaccine annually any
tuberculosis (Mantoux positive) isoniazid 300 mg/pyridoxine for 9 months any
toms and signs should raise alarm bells and trig-
ger investigation of an HIV-related infection or
malignancy. Signs or symptoms which warrant
further investigation include: persistent constitu-
tional symptoms of unexplained weight loss,
fatigue, malaise, fever, sweats, diarrhoea; skin
conditions such as seborrheic dermatitis and
eosinophilic folliculitis; respiratory complaints of
dry cough and dyspnoea; neurological symptoms
of headache, seizure, weakness, numbness, visual
disturbances and psychiatric changes including
the development of depression, sleep distur-
bances, memory problems and slowed reaction
times or hypomania. If the patient develops unex-
plained symptoms or signs in the setting of
immunodeciency, it is important to contact an
infectious diseases or HIV specialist for referral
and/or guidance on investigation and manage-
ment.
Summary
Given the long period of clinical latency typically
seen in HIV disease, primary care management of
HIV disease is often highly appropriate despite
the increasing complexity of antiretroviral man-
agement. Monitoring of disease progression
should focus on clinical, immunological or viro-
logical markers of disease progression. Referral to
a specialist HIV antiretroviral prescriber (GP or
physician) should be made when signs of disease
progression occur. Psychosocial management, safe
sex education and provision of information and
referral are key features of HIV/AIDS primary
management.
References
1 Kent SJ and Pierce A. Routine vaccinations for HIV-1
infected adults. Position Paper. Australasian Society
for HIV Medicine; February, 2001.
2 Mellors JW, Rinaldo CR, Gupta P, et al. Prognosis in
HIV-1 infection predicted by the quantity of virus in
plasma. Science 1996; 272: 1167-1170.
3 Mellors JW, Munoz AM, Giorgi JV. Plasma viral load
and CD4+ lymphocytes as prognostic markers of
HIV-1 infection. Ann Intern Med 1997;126:946-954.
4 Saag MS, Holodniy M, Kuritzkes DR, et al. HIV viral
load markers in clinical practice. Nat Med
1996;2:625-629.
5 Clinical Trials and Treatments Advisory Committee
to the Australian National Council on AIDS and
Related Diseases. Model of Care for HIV infection in
Adults. Canberra: Department of Health and Aged
Care; 2001.
6 Adapted from material originally submitted by G.
Rogers et al, Chapter 6.
7 Komiti A, Hoy J, Judd F, et al. Depression in HIV infected
patients attending general practice clinics. 12th Annual
Conference of the Australasian Society for HIV
Medicine: 2000 12-14 Oct; Melbourne. Abstract P32.
8 Rogers G, Curry M, Oddy J, Beilby J. Serious health
disadvantage evident in a cohort of HIV positive and
HIV negative gay men: baseline health
characteristics of the care and prevention
programme cohort. 12th Annual Conference of the
Australasian Society for HIV Medicine: 2000 12-14
Oct; Melbourne. Abstract P56.
9 Grierson J, Bartos M, de Visser R, McDonald K.
Futures II: The health and well-being of people with
HIV/AIDS in Australia. Monograph Series Number 17.
Melbourne: Australian Research Centre in Sex,
Health and Society, La Trobe University; 2000.
10 Palella FJ Jnr, Delaney KM, Moorman AC, et al.
Declining morbidity and mortality among patients
with advanced human immunodeciency virus
infection. HIV Outpatient Study Investigators. N Engl
J Med 1998;338:853-860.
11 Marschner IC, Collier AC, Coombs RW, et al. Use of
changes in plasma levels of human
immunodeciency virus type 1 RNA to assess the
clinical benet of antiretroviral therapy. J Infect Dis
1998;177:40-47.
12 US Department of Health and Human Services
Panel on Clinical Practices for Treatment of HIV
Infection. Guidelines for the Use of Antiretroviral
Agents in HIV-infected Adults and Adolescents. April
2001. http://www.hivatis.org
13 British HIV Association Writing Committee. Draft
British HIV Association (BHIVA) guidelines for the
treatment of HIV-infected adults with antiretroviral
therapy. 2001. http://www.aidsmap.com
14 Carpenter CC, Cooper DA, Fischl MA, et al.
Antiretroviral therapy in adults. Updated
recommendations from the International AIDS
Society USA Panel. JAMA 2000;283:381-390.
15 Carr A, Cooper DA. Adverse effects of antiretroviral
therapy. Lancet 2000;356:1423-1430.
16 Carr A, Miller J, Law M, Cooper DA. A syndrome of
lipoatrophy, lactic acidemia and liver dysfunction
associated with HIV nucleoside analogue therapy:
contribution to protease inhibitor-related
lipodystrophy syndrome. AIDS 2000;14:F25-32.
17 Chesney MA. Factors affecting adherence to
antiretroviral therapy. Clin Infect Dis 2000;30(suppl
2):171-176.
18 Condra JH, Petropoulos CJ, Ziermann R, et al. Drug
resistance and predicted virologic responses to
human immunodeciency virus type 1 protease
inhibitor therapy. J Infect Dis 2000;182:758-765.
19 Emery S, Capra WB, Cooper DA, et al. Pooled
analysis of 3 randomized, controlled trials of
Interleukin-2 therapy in adult human
immunodeciency virus type 1 disease. J Infect Dis
2000;182:428-434.
20 USPHS/IDS. Guidelines for the prevention of
opportunistic infections in persons infected with
human immunodeciency virus. MMWR 1999:48:
1-67.
10
Primary care management of
Robert Feller Hepatologist, Central Sydney Area Health Service, New South Wales.
Simone Strasser Hepatologist, Central Sydney Area Health Service, New South Wales.
Jeff Ward Executive Ofcer, Hepatitis C Council of Queensland.
Gillian Deakin General Practitioner, Bondi, New South Wales.
Introduction
A primary care role in the management of chronic
viral hepatitis involves the provision of informa-
tion, support and referral as well as initial and
ongoing clinical assessment and monitoring. The
primary care clinician may undertake tasks such
as specic diagnosis and initial assessment of the
severity of disease, counselling the patient about
the current understanding of the disease process
and potential complications, as well as general
issues of diet, mental health, lifestyle, transmission
and vaccination.
1,2
With recent advances in the
treatment of hepatitis B and C, the primary care
clinician has an important role in presenting the
patient with specic treatment options and poten-
tial side-effects.
3
This chapter focuses on the pri-
mary care management of chronic hepatitis C,
with some consideration of treatment options for
chronic hepatitis B.
Clinical evaluation
Diagnosis
The initial approach of the clinician must include
consideration of the non-viral and viral aetiologies
for hepatitis (Table 10.1). Elevated liver enzymes are
often a trigger for consideration of viral hepatitis.
The most common causes of abnormal liver func-
tion tests (LFTs) seen in clinical practice include
fatty liver, alcoholic liver disease and drug toxicity
(usually transient) as well as chronic viral hepatitis.
A diagnosis of chronic hepatitis requires persis-
tently abnormal liver function tests for a period of
six months. Thus, the strict denition is one of
duration rather than severity (Chapters 5 and 7).
The majority of patients with chronic viral
hepatitis will be asymptomatic or have non-spe-
cic symptoms such as fatigue and lethargy, and
only some will have signs of compensated or
Key points
Patients with active chronic viral hepatitis should be monitored
every six months. Liver biopsy is the denitive investigation to
assess the degree of hepatic inammation, brosis and
cirrhosis.
Effective antiviral therapy is available for chronic hepatitis B
and C in some patients.
For patients with chronic hepatitis C, the rate of progression to
cirrhosis is usually very slow and antiviral treatment is not
indicated in all cases.
Most patients with adult-acquired chronic hepatitis B infection
will not suffer long-term sequelae but approximately 25% of
people with chronic hepatitis B from infancy develop cirrhosis
or hepatocellular cancer. Antiviral treatment is indicated in
many patients with active chronic replicative hepatitis B.
Depending on viral genotype and other cofactors, between
3070% of patients have a sustained response to currently
approved HCV treatments.
A course of antiviral treatment for HBV can induce sustained
HBeAg seroconversion in 3050% of patients, as well as
clinical improvements and survival benets. Potential benets
of antiviral therapy for chronic hepatitis B include e antigen
seroconversion, improved liver function, improved liver
histology and reduced progression to cirrhosis and its
complications.
Primary care management of chronic viral hepatitis includes
education and counselling, psychosocial support and dietary
and lifestyle advice. It also involves monitoring the disease
process and identifying if and when referral to a specialist is
required.
Prevention education and vaccination against other hepatitis
viruses are important in the management of chronic viral
hepatitis.
decompensated cirrhosis. Chapter 7 contains a
detailed discussion of the clinical presentation of
chronic viral hepatitis.
A sound understanding of modes of transmis-
sion, risk behaviours and epidemiology should
permit a detailed risk assessment in patients with
suspected hepatitis of unknown aetiology
(Chapters 13). In cases where clinical and risk
assessment suggest the possibility of viral hepati-
tis, viral serology should include anti-HAV IgM,
HBsAg, HCV antibody (anti-HCV) and HIV anti-
body (anti-HIV), as appropriate, following pre-
test counselling and informed consent (Chapter
8). Patients with advanced HIV infection may lose
anti-HCV reactivity. Therefore, serum HCV RNA
should be assessed if acute or chronic HCV infec-
tion is suspected in HIV patients with negative
antibody results.
Further considerations are dependent upon
whether the patient has chronic HCV or chronic
HBV infection.
Hepatitis C
Initial assessment
A detailed history should include an estimation of
the duration of exposure, age at infection and
whether there are important contributing factors
to hepatic brosis. These factors may include a
history of signicant alcohol consumption, obesity
and diabetes, which are risk factors for non-alco-
holic fatty liver disease. Concomitantly, the
patient should be evaluated for ongoing risks,
such as injecting drug use and ongoing, excessive
alcohol consumption.
Initial assessment of a patient with hepatitis C
should address whether or not the patient has
active disease, inactive disease or has cleared
infection. Chapter 7 discusses virological markers,
liver function tests, liver imaging, liver biopsy and
other investigations which form the basis of this
assessment.
Patients found to have elevation of serum ALT
levels should have liver tests monitored monthly
for several months to establish whether there is a
persistent elevation of ALT. If persistent ALT ele-
vation is identied, patients should be carefully
evaluated to determine the severity of disease.
If ALT levels and other enzymes are normal,
patients should be assessed for the presence of
viraemia by polymerase chain reaction (PCR).
The HCV PCR test is rebatable under Medicare
for this indication. Patients found to be HCV
RNA negative should be reassured that while they
have probably been exposed to HCV in the past,
they have apparently cleared infection. It is rec-
ommended that patients with normal liver func-
tion and no detectable HCV RNA have their liver
enzymes checked one year after initial evaluation;
if HCV RNA remains negative and liver enzymes
are normal, no further follow-up is necessary.
Patients with normal ALT levels who are HCV
RNA positive should be followed on an annual
basis, as ares of activity may be observed.
See Tables 10.2 and 5.5 for a summary of
serological and virological markers.
Ongoing monitoring of patients with
chronic hepatitis C
The aims of follow-up in patients with chronic
hepatitis C are to:
reinforce the need for lifestyle changes;
decide which patients are appropriate for
antiviral therapy;
determine appropriate timing of referral to a
specialist;
monitor patients with cirrhosis for
complications such as hepatic
decompensation or hepatocellular carcinoma.
TABLE 10.1 Important causes of chronic hepatitis
Aetiology Diagnostic test
Fatty liver (incl. non-alcoholic Risk factors, imaging biopsy
steatohepatitis)
Alcohol History biopsy
Viral
Hepatitis B Viral serology (Tables 10.3 and
Hepatitis C 5.5)
(Hepatitis D)
Metabolic
Haemochromatosis Iron studies, HFE gene test
Wilsons disease Serum copper, caeruloplasmin
Alpha-1-antitrypsin deciency Serum alpha-1-antitrypsin
Autoimmune hepatitis Anti-nuclear antibody(ANA),
anti-smooth muscle antibody (SMA),
immunoglobulins and biopsy
Drugs History biopsy
Cryptogenic
For patients with chronic hepatitis C, ongoing
monitoring is recommended every six months,
unless there are specic reasons for more frequent
monitoring (e.g. encouraging behaviour change).
Tests to be conducted may include:
liver function tests;
full blood count;
prothrombin time or INR;
hepatic ultrasound (in patients with cirrhosis);
liver biopsy (if treatment is being considered).
Assessment for antiviral therapy
Antiviral therapy is funded for patients at highest
risk of histologic progression who are most likely
to benet from viral eradication. Assessment of
patients for antiviral therapy involves an evalua-
tion of current disease severity and their risk of
progression to fibrosis and cirrhosis. Clinical
examination should be conducted (Chapter 7)
and the investigations listed above should be per-
formed.
The nding of an elevated ALT indicates the
presence of necroinammatory activity but is not
predictive of cirrhosis or significant fibrosis.
Thrombocytopenia, prolonged INR or hypoalbu-
minaemia all suggest the presence of cirrhosis
with some degree of hepatic decompensation and
portal hypertension. However, patients with well-
compensated cirrhosis due to hepatitis C may
have a completely normal platelet count, INR and
serum albumin level for many years. Hepatic
ultrasound may show features of cirrhosis or fatty
inltration but is commonly normal.
When assessing a patient for antiviral therapy,
a liver biopsy is recommended. Liver biopsy is the
denitive way to document the degree of hepatic
inammation, brosis and cirrhosis, as currently
there are no reliable non-invasive methods for
predicting these features. Currently, a liver biopsy
is mandatory for accessing funded antiviral treat-
ment under the Section 100 of the Pharmaceutical
Benefits Scheme (PBS) for highly specialised
drugs.
Liver biopsy is a relatively safe procedure. It is
usually performed as a day-stay procedure, under
ultrasound guidance using local anaesthetic only.
Patients commonly experience some minor
abdominal discomfort and right shoulder tip pain
but severe pain is unusual. There is a small risk of
signicant bleeding (1:300) and death (1:10,000).
There are several systems in use for recording
the degree of brosis in a liver biopsy. Most of
these systems use a scoring system ranging from 0
(no brosis) to 4 (denite cirrhosis). The nding
of minimal disease activity and no brosis (stage
0) suggests a very low likelihood of disease pro-
gression. Consequently, the patient may be reas-
sured and toxic and expensive therapy may be
avoided. Patients with stage 1 fibrosis may be
offered antiviral therapy if there is associated
moderatesevere inflammation, while patients
with stage 24 brosis should be offered antiviral
TABLE 10.2 Interpretation of HBV, HCV and HDV serology
Virus Marker Signicance
Hepatitis B (HBV) HBsAg Persistent infection
anti-HBs Past infection (natural immunity) or vaccination (acquired immunity)
HBeAg Highly infectious (absence may indicate mutant form)
anti-HBc IgM Recent/current infection*
anti-HBc IgG Past infection (current if sAg positive)
HBV DNA Circulating virus (copies/ml)
Hepatitis C (HCV) anti-HCV Current or past infection
HCV RNA Circulating virus (copies/ml)** indicating current infection
Hepatitis D (HDV) anti-HDV Current or past infection (co-exists with HBV)
Ag = antigen; s = surface; c = core; anti = antibody.
*May be only indicator of infection in window period between disappearance of sAg and appearance of sAb.
**May be useful in high-risk HCV antibody-negative patient.
10 Primary care management of chronic viral hepatitis
therapy, provided no contraindications are pre-
sent. Consideration of duration of infection is also
important in the assessment of disease severity,
rate of progression and need for treatment. For
example, patients who have stage 1 brosis after
three years of infection may have greater need for
treatment than a person with stage 1 brosis after
ten years.
Viral genotype impacts on length of treatment
and likely response and, as discussed in the treat-
ment section, genotype testing may assist the
patient in making the decision to start treatment.
Alternatively, genotype testing may be delayed
until the patient sees a hepatologist.
In determining whether a patient is appropri-
ate for antiviral treatment, the primary care clini-
cian may also consider the patients social support
and whether he/she is likely to adhere to treat-
ment. The local hepatitis C council or drug user
group may provide information and peer support
for people considering treatment (Chapter 14).
Shared care and referral
The primary care clinician has an important role
in assessing which patients with chronic hepatitis
C should be referred for specialist review. Such
patients include those with persistently elevated
ALT levels who may be appropriate for antiviral
therapy, those with clinical or laboratory features
suggestive of cirrhosis, and those who request spe-
cialist evaluation. Table 10.3 outlines investiga-
tions to conduct prior to referral. Referral to a
liver clinic or hepatologist, which can be made at
any time, is necessary for liver biopsy and special-
ist pre-treatment assessment. Ongoing support
and management of the patient on treatment may
be conducted by primary care clinicians and spe-
cialists in a shared care setting.
Monitoring for complications of liver disease
Patients with HCV-associated cirrhosis should be
monitored for deteriorating liver function and for
the development of hepatocellular carcinoma.
Often a specialist is involved in the care of a
patient with cirrhosis but frequently the patient
will attend his/her general practitioner when new
symptoms develop. Concerning features include:
falling serum albumin levels;
prolongation of prothrombin time;
development of jaundice;
development of other clinical signs (e.g.
peripheral oedema, ascites, muscle wasting).
Patients with these features should be considered
for referral to a liver transplant unit.
Hepatocellular carcinoma is becoming a major
clinical problem in patients with HCV-associated
cirrhosis. The current recommendations regard-
ing screening for hepatocellular carcinoma
include ultrasound and alpha-foetoprotein levels
every six months, to detect small lesions amenable
to curative treatment.
Hepatitis B
Initial assessment
The natural history of HBV infection varies
according to age at acquisition of infection, mode
of transmission and ethnic background. In people
infected since infancy, hepatitis B proceeds
through fairly predictable stages: a prolonged
immunotolerant phase; a phase of attempted
immune-mediated clearance, and then a quiescent
phase. Not all patients pass through the immune-
clearance phase, and some can continue to have
hepatitic ares for many years, particularly if an
HBeAg-negative (pre-core) mutant emerges
(Chapter 1).
The aim of the initial evaluation of a patient
with chronic hepatitis B is to assess the stage and
severity of disease. Full viral serology and other
investigations to be conducted during initial
assessment are discussed in detail in Chapter 7.
Serology results (Table 10.2) should be
assessed in the context of liver function and the
age of the patient. For example, a patient aged less
than 20 years who is positive for surface and e
antigen (HBsAg+ and HBeAg+) and has normal
liver enzymes does not require antiviral therapy.
However, this patient should be told that he/she
has a high likelihood of developing flares of
hepatitis over subsequent years. Follow-up should
be recommended so that hepatitis ares can be
identied and antiviral treatment be given at an
appropriate time.
Patients over 20 years with abnormal liver
function tests should have HBeAg status checked.
If HBeAg+, they have active infection with wild-
type HBV. If HBeAg is negative, they have a high
likelihood of infection with an HBeAg-negative
mutant. In this situation, HBV DNA should be per-
formed to determine if viraemia is present. If HBV
DNA is negative, and the patient has abnormal
LFTs, alternative diagnoses should be considered.
HBsAg+, HBeAg-negative and anti-HBe+
patients with normal liver enzymes are in a rela-
tively inactive phase of disease, although they may
already be cirrhotic.
Patients with HBeAg-negative disease (pre-core
mutant) should be considered for antiviral therapy
if liver enzymes are uctuating, as they have a high
likelihood of progressing to cirrhosis. Patients with
known cirrhosis without decompensation should
also be considered for antiviral therapy as there is
evidence of reduced progression to decompensated
liver disease and HCC.
General management issues for
patients with viral hepatitis
Discussion about routes of
viral transmission
Patients with viral hepatitis will commonly be
concerned about the risks of transmitting the
infection to others. Issues regarding sexual trans-
mission, mother-to-child transmission, blood-
borne transmission and casual contact transmis-
sion should all be discussed.
Hepatitis C is transmitted primarily through
blood-to-blood contact. The sharing of grooming
tools that can cause skin abrasion (such as razors,
toothbrushes and tweezers) should be avoided.
Injecting drug users must be encouraged to use
sterile water, needles and syringes, as well as new
injecting equipment such as spoons, lters and
tourniquets each time they inject (Chapter 3 and
Appendix 4).
Patients may be concerned about sexual trans-
mission of HCV. There appears to be a very low
risk of sexual transmission of HCV, although sex-
ual behaviours that potentially involve exposure
to HCV-infected blood may pose a more signi-
cant risk. There is conicting evidence concerning
an increased risk of HCV transmission during
anal intercourse and condoms may be recom-
mended in this context.
There clearly is a risk of transmitting HCV
from mother to child, although the risk is low
(approximately 5%).
4
This risk is significantly
higher if the mother is coinfected with HIV.
Currently, there is no indication for elective cae-
sarean section in HCV-positive mothers.
However, it should be noted that there is some
evidence that prolonged rupture of membranes
and use of invasive foetal monitoring may
increase the risk of mother-to-child transmission
of HCV
5
, and decisions about intervention may
need to be made on a case-by-case basis. Breast-
feeding is not generally considered to present an
additional risk of HCV transmission. However,
breast-feeding should be suspended if the nipples
are cracked or if the baby has cuts in or outside
the mouth.
Ongoing monitoring of patients with
chronic hepatitis B
All HBsAg+ patients should be followed, regard-
less of their apparent virologic status at initial
evaluation. The six monthly review of patients
with chronic hepatitis B includes:
a check for signs of chronic liver disease or
decompensation;
serum liver function tests, FBC, coagulation
studies and alpha foetoprotein;
liver ultrasound if cirrhotic or family history
of HCC.
HBsAg+, HBeAg-negative females with no evi-
dence of active liver disease are generally at low
risk of progression and require only yearly check-
ups to make sure that their status has not
changed. For reasons that remain unclear, males
with the same serologic status, particularly those
with infection since infancy, remain at risk of
HCC development regardless of the presence or
absence of cirrhosis. They should be seen twice a
year for review.
Patients with known cirrhosis should undergo
serum alpha-foetoprotein assessment and ultra-
sound every six months to screen for HCC.
Because non-cirrhotic patients are also at risk of
HCC, screening is recommended by some physi-
cians but this policy is not universally adopted.
Patients with active liver disease (that is, with
abnormal liver enzymes) should be closely moni-
tored and considered for antiviral therapy. In
HBeAg+ patients, the long-term response to
antiviral therapy is signicantly better if treatment
is initiated during a hepatitic are (ALT > 2 times
normal) rather than when enzymes are normal or
only mildly elevated (ALT < twice normal).
TABLE 10.3 Pre-referral investigation checklist
Liver function tests (usually 3 tests are conducted over 6 months)
HCV serology (anti-HCV)
HBV serology (HBsAg, anti-HBs, HBeAg, anti-HBc)
HAV serology
HIV serology
FBC, electrolytes, creatinine, coagulation studies (INR/APTT)
Alpha foetoprotein
Liver ultrasound
In Australia, many HBV-infected individuals
are migrants who contracted infection as infants.
With universal HBV vaccination of neonates and
administration of hepatitis B immunoglobulin to
infants of HBV-infected mothers, there are very few
new cases of vertically acquired HBV in Australia.
Most cases are acquired sexually or through direct
blood-to-blood contact. HBV-infected individuals
should ensure the safety of sexual partners by rec-
ommending vaccination and using safe-sex meth-
ods. Any patient who is HBsAg+ may transmit
HBV sexually. Other recommendations to prevent
blood-to-blood HBV transmission are as for pre-
vention of HCV transmission.
Risk of transmission/infection is discussed in
detail in Chapter 2. Communication of safe sex
and safe injecting messages is covered in Chapter
3 and Appendices.
Lifestyle issues
The possibility of lifestyle modication needs to
be discussed with the patient, particularly in rela-
tion to alcohol consumption and recreational
drug use.
Alcohol intake should be minimal. There is no
doubt that excessive alcohol consumption (>50
g/day) leads to disease progression and a poorer
response to treatment in chronic HCV. (A drink
containing 10 grams of alcohol is regarded as a
standard drink. A can of regular beer contains
approximately 15 grams, a bottle of wine contains
7080 grams and a nip of spirits contains 10
grams of alcohol.
6
) Australian guidelines published
by the Digestive Health Foundation recommend
that people with viral hepatitis should drink alco-
hol infrequently or at low levels, and should
consider not drinking at all. Specic strategies are
set out in Table 10.4. Individuals with cirrhosis
should be encouraged to stop drinking alcohol.
Individuals who continue to inject drugs are of
particular concern. Those using in a chaotic man-
ner, particularly in an unsafe environment, are less
at risk from chronic hepatitis C infection than
from major overdose, acquisition of other viral
infections, and other health concerns. In such
patients, these areas should be the focus of atten-
tion, rather than the presence of chronic hepatitis
B or C. Referral to treatment programs and sup-
port groups may be appropriate.
Nutrition
There is considerable, unsubstantiated dietary
information and advice directed at people with
chronic viral hepatitis. In November 2000, the
Dietitians Association of Australia supported
dietary advice for people with hepatitis C. This
advice strongly warns against restrictive diets
which recommend exclusion of all dairy foods,
red meat, caffeine-containing drinks, and food
containing added sugar, artificial colours and
preservatives.
7
Instead, a well-balanced diet is rec-
ommended. For most people with hepatitis C,
dietary recommendations are the same as for the
general population (encouraging: grilled rather
than fried food; lean meats and sh; reduced-fat
products; wholemeal bread; vegetables and fruit;
pasta; minimisation of fat for spreading and cook-
ing). People with advanced liver disease, or other
conditions such as coeliac disease or diabetes may
be referred to a specialist dietitian for further
advice.
Overweight or obese patients should be
advised of a gradual weight-reduction program,
particularly as there is increasing evidence of
interaction between HCV, obesity and type 2 dia-
betes in accelerating progression to brosis. Those
who may have fatty liver need to avoid a precipi-
tous fall in weight as this can induce deterioration
in liver function.
Many people with active hepatitis C report
nausea and intolerance to certain foods and
drinks. Referral to a dietitian may be appropriate
to ensure the patient is consuming necessary vita-
mins and minerals.
Patients with advanced liver disease who
develop protein-calorie malnutrition should be
seen by a specialist dietitian. Such patients often
require protein supplementation, and should be
encouraged to eat high-energy foods frequently
throughout the day. Very few, if any, patients with
advanced liver disease should be subjected to pro-
tein restriction. This is a change from the previous
doctrine that all patients with hepatic
encephalopathy should be protein restricted.
TABLE 10.4 How to reduce alcohol consumption
Plan at least two alcohol-free days per week
Switch to low alcohol or alcohol-free drinks
Avoid situations where there will be pressure to drink, e.g.
rounds at the pub
Alternate non-alcoholic and alcoholic drinks
Drink a daily maximum of two drinks
Fatigue and other symptoms
People with chronic hepatitis C may report fatigue,
malaise, headache, rash, and aching muscles and
joints. Consideration should be given to specic
food and drinks that may be triggering symptoms,
as well as work, family or other commitments,
which may exacerbate stress and fatigue. Patients
may benet from planning rest periods during the
day or incorporating light-to-moderate exercise
into their routines to reduce fatigue.
For reasons that are unexplained, patients
with chronic hepatitis B infection seem to experi-
ence less fatigue than patients with chronic hepati-
tis C, unless they are having a hepatitic are.
Vaccination
Coinfection with more than one hepatitis virus
may be associated with more severe liver disease.
Superinfection with hepatitis A infection (HAV) in
a patient with chronic hepatitis B or C, or acute
hepatitis B in a patient with chronic hepatitis C
may precipitate the development of acute liver
failure. In the long term, patients with HBV and
HCV coinfection tend to be more likely to
progress to cirrhosis and to develop hepatocellu-
lar carcinoma. Thus, HAV and HBV vaccination
should be offered to all patients with chronic
hepatitis C, and HAV vaccination should be
offered to chronic hepatitis B patients (Chapter 5).
Psychosocial support
Patients may experience social isolation, anxiety
or discrimination related to infection with viral
hepatitis, which may be compounded by physical
symptoms. The primary care clinician can begin
by listening to the patient and demonstrating sen-
sitivity to linguistic and cultural differences, which
may impact on an individuals response to viral
hepatitis. Provision of verbal and written infor-
mation relating to transmission or disease natural
history may allay fears (Chapter 14).
Referral to counselling or support services
may be indicated for patients with complex emo-
tional, family/relationship or disclosure issues. All
patients should be made aware of services such as
counselling and support groups, telephone
helplines and community organisations.
Information about services is available from any
teaching hospital unit or the local hepatitis C
council (Chapter 14).
Complementary therapies
There is little evidence that herbal medicines have
a profound antiviral effect despite many patients
reporting some symptomatic improvement and
the ability of some agents to induce a fall in ALT.
8,9
Most preparations are safe but some have repor-
ted hepatotoxicity and should be avoided (e.g.
mistletoe, valerian, heliotropium, kombucha tea).
Close monitoring of liver biochemistry is recom-
mended at the commencement of any herbal med-
icine.
Steroids and viral hepatitis
Severe ares of hepatitic activity may be seen fol-
lowing a course of corticosteroids or other
immunosuppressive or cytotoxic therapy, particu-
larly in patients with chronic hepatitis B. Such
ares may be fatal. For instance, HBsAg+ patients
receiving chemotherapy have a 5% mortality
from acute liver failure. People with HCV infec-
tion may also have mild ares of activity in such
circumstances. However, acute liver failure does
not occur.
Antiviral therapy for viral hepatitis
Aims of treatment
There are a number of aims of antiviral therapy in
chronic viral hepatitis. These include:
eradication of infection;
prevention of disease progression;
improvement in histologic markers;
improvement of symptoms;
improved survival.
All these aims can be achieved in a signicant pro-
portion of patients with hepatitis C or hepatitis B
with currently available therapies.
Antiviral therapy Hepatitis C
The major aim of treatment is to achieve viral
eradication. In hepatitis C, viral eradication is
dened by the achievement of a sustained virolog-
ical response (SR); that is, negative HCV RNA
and normal ALT values six months after the com-
pletion of six or twelve months of therapy.
The most effective therapy for hepatitis C is a
combination of once-weekly subcutaneously
administered pegylated interferon plus twice-daily
oral ribavirin. Such treatment is available in
Australia under Section 100 of the PBS (Table
10.5). The combination of pegylated interferon
TABLE 10.5 Treatments for hepatitis B and C. Section 100 Highly Specialised Drugs Program of the PBS**
Treatment Condition Criteria Caution
Lamivudine (Zefx) Chronic Histological evidence of chronic
100mg daily taken orally hepatitis B hepatitis B on liver biopsy*
Abnormal serum ALT levels
HBeAg positive and/or HBVDNA positive
Absence of pregnancy and lactation
Female patients using effective
contraception
Persons with advanced liver disease
should have their treatment discussed
with a transplant unit prior to initiating
therapy
Interferon alfa-2a (Roferon-A) Chronic Chronic hepatitis B on liver biopsy*
Interferon alfa-2b (Intron A) hepatitis B HBeAg+ and/or HBV DNA+
5-10 million units HBV infection > 6 months
subcutaneously 3 times weekly Abnormal ALT
for 16-24 weeks Absence of class B or C
cirrhosis (ascites, variceal
bleeding, encephalopathy,
albumin<30 g/l, bilirubin>30
mmol/l
Absence of pregnancy and
lactation
Female patients using effective
contraception
Pegylated Interferon alfa-2a Chronic Biopsy showing stage 24
plus Ribavirin (PegasysRBV hepatitis C brosis or stage 1 brosis plus
Combination Therapy) with moderate to severe inammation*
Pegylated Interferon alfa-2b compensated Abnormal ALTs plus anti-HCV+
plus Ribavirin (Pegatron liver disease. and HCV RNA+
Combination Therapy) No prior Absence of pregnancy and
Patients with genotype 1, 4, 5 or interferon or lactation in women
6 or genotype 2/3 with cirrhosis peg-interferon Patient (male or female) and
or bridging brosis may have his/her partner must use effective
treatment for 48 weeks. Patients forms of contraception (one for
with genotype 1, 4, 5 or 6 may each partner)
only continue treatment beyond 12
weeks if HCV RNA is negative or
viral load has dropped by at least
2 logs. For patients with genotype
2 or 3 without cirrhosis or bridging
brosis the treatment course is
limited to 24 weeks. Patients with
genotype 2 or 3 with cirrhosis or
bridging brosis may only continue
treatment after 24 weeks if HCV
RNA is not detectable by
PCR assay.
*Patients with severe coagulation disorders not required to undergo biopsy.
**Details correct at February 2004. Reference to updated guidelines is advised.
The development of
lamivudine resistance in
patients with cirrhosis or who
are immunosuppressed may
be associated with a severe
are of hepatitis and
progression to liver failure.
Interferon alfa has been
associated with depression
and suicide. Patients with a
history of mental illness
should be warned of the
risks. Psychiatric status must
be monitored during therapy.
As for interferon above
Ribavirin is a category X drug
and must not be given to
pregnant women.
Pregnancy in women taking
ribavirin and in the female
partners of men taking
ribavirin must be avoided
during treatment and for 6
months following treatment.
and ribavirin produces an overall SR of greater
than 50%,
10,11
a signicant improvement over the
SVR rates achieved with interferon monotherapy
(<10%) or standard interferon (given three times
a week) plus ribavirin (40%).
The likelihood of response is much higher in
patients infected with genotype 2 or 3 (80% SR
rate after six months of combination pegylated
interferon/ribavirin) than genotype 1 or 4 (50% SR
rate after 12 months of therapy). While HCV
genotype is the most powerful predictor of
response, other predictors of SR include low viral
load, minimal hepatic brosis, female gender and
age (younger than 40 years). The benefits
of achieving an SR include a reduced risk of
progression for patients at all stages of disease and
probably a lower incidence of HCC develop-
ment. In addition, there have been reports of sig-
nicant regression of brosis, even in cirrhotic
patients.
Patients who relapse after initially responding
to monotherapy should be offered treatment with
combination interferon and ribavirin, as response
rates in this group are equivalent to those seen in
untreated patients. Patients who have failed to
respond to either interferon monotherapy or com-
bination therapy are not eligible for further treat-
ment under current Section 100 guidelines but
may pay for their own treatment, or access newer
treatments such as pegylated interferon through
hospitals offering treatment through expanded
access protocols.
Therapy may be for six or twelve months
duration, depending on HCV genotype.
12
When
discussing the benets and risks of treatment, the
general practitioner can request genotype testing.
Medicare funding covers genotype testing. This
information may help to guide a patient who is
somewhat ambivalent about having treatment. In
particular, patients with genotype 2 or 3 can be
counselled that they have a high chance of eradi-
cating the virus with six months of treatment.
Patients with genotype 1 infection can also be
informed of their likelihood of eradicating infec-
tion. While this rate is lower, it should not dis-
suade patients from attempting treatment but
remains an important discussion point. These dis-
cussions may take place before specialist referral.
There is a signicant number of patients with
hepatitis C who respond poorly to therapies or
have contraindications to therapy. Decisions
about therapy in these individuals are made on a
case-by-case basis by the specialist. These include
patients with HCV/HBV coinfection, HCV/HIV
coinfection, chronic renal failure, cryoglobulin-
aemia and with HCV recurrence after liver trans-
plantation.
HIV/HCV coinfection
HIV/HCV coinfection is associated with higher
HCV viral load and an accelerated rate of HCV
disease progression.
13
There is no fundamental
difference to the management of HCV in the pres-
ence of HIV. Patients with HIV/HCV coinfection
who have stable CD4 cell counts on antiretroviral
therapy, with ongoing evidence of active HCV,
may be considered for combination interferon
plus ribavirin. Such management is difcult, par-
ticularly in patients already taking multiple med-
ications, as side-effects, drug interactions and
poor tolerability are common.
14
Who should be treated for hepatitis C?
Antiviral therapy is currently recommended for
patients with:
elevated ALT values for six months;
detectable serum HCV RNA;
compensated liver disease and signicant
inammation and/or brosis on liver biopsy.
Table 10.5 details who can receive treatment for
hepatitis C through Section 100 of the PBS.
The major contraindications to therapy
include:
decompensated liver disease;
major psychiatric conditions, particularly
severe depression;
autoimmune disease;
signicant cardiac disease;
pregnancy. (Ribavirin is a teratogen. Patients
and their partners must avoid pregnancy
during therapy and for six months after
cessation of treatment due to the possibility of
birth defects.)
Although interferon is contraindicated in people
with depression it may be used safely in patients
with controlled depression/anxiety disorders or
controlled seizure disorders. If the patient is being
treated by a psychiatrist or neurologist, discussion
with the specialist is recommended before the ini-
tiation of interferon therapy.
Side-effects
Side-effects are common but do not usually require
discontinuation of treatment. However, patients do
require signicant support and encouragement
throughout treatment. Adverse effects of therapy
include u-like symptoms, irritability, weight loss,
insomnia, vomiting, depression and anxiety, mild
hair loss, rash, cough, myelosuppression and induc-
tion of autoimmunity, particularly thyroid disease.
Ribavirin treatment always induces a degree of
intravascular haemolysis, which results in a fall in
haemoglobin in most patients. This anaemia may
result in tiredness, shortness of breath and precipita-
tion of myocardial ischaemia in at-risk patients.
Depression may occur as a result of serotonin deple-
tion caused by interferon, and SSRIs may be consid-
ered for management or prophylaxis.
Given the wide range and potential serious-
ness of side-effects, patients must be closely moni-
tored during therapy. Currently, most treatment is
provided through public hospitals and patients
have ready access to nurse specialists to advise
and support them through therapy. In general,
patients on therapy are seen once a week for the
rst month, and then each month until the end of
treatment, with blood counts and biochemistry
evaluated at each visit. Dose modication guide-
lines are followed when side-effects or laboratory
changes require intervention.
The decision to treat
Given the likelihood of signicant side-effects,
decisions about whether to treat and when to
treat are often difcult. When discussing therapy
with a patient, issues and commitments such as
work, study, relationships, substance abuse and
pregnancy should be considered.
The shift to primary care
While most treatment is based in public hospitals
at present, there is an important trend towards
treatment in the community. This will involve pri-
mary care clinicians taking on a greater role in the
support and monitoring of patients on therapy.
Many hospitals have put together shared-care
packages with specic information and guidelines
about management during therapy. In addition, a
small number of GPs in NSW and ACT have been
approved to prescribe combination therapy as
part of a S100 community prescribing pilot pro-
ject. To ensure the highest chance of achieving
viral eradication, it is important to support
patients through a complete course of therapy.
Antiviral therapy Hepatitis B
The first treatment available for patients with
chronic hepatitis B was interferon alfa (see Table
10.5). Recently, the nucleoside analogue lamivu-
dine has become available for the treatment of
hepatitis B through Section 100 of the PBS.
15,16
A 46 month course of interferon is associated
with HBeAg loss in 3040% of patients and, in
early trials, approximately 10% lost HBsAg.
17,18
Long-term benets include improved survival and
a reduction in the incidence of HCC. Interferon is
of particular benet in those patients with high
ALT and low HBV DNA levels but is ineffective
against HBeAg-negative mutant HBV. Interferon
may be hazardous to those with advanced liver
disease and is associated with significant side-
effects.
Lamivudine (100 mg daily) is highly effective
in suppressing HBV replication and improving
liver histology. The rate of HBeAg seroconversion
after 12 months of lamivudine therapy is compa-
rable to that after 46 months of interferon, and
increases with longer treatment to over 70% at
four years.
19
It is very effective against HBeAg-
negative mutant HBV and is useful in both com-
pensated and decompensated cirrhosis. Cessation
of lamivudine treatment is, however, frequently
associated with virological and biochemical
relapse. Unfortunately, lamivudine therapy is also
associated with the emergence of resistant strains
(YMDD variants), and incidence of mutations
increases with duration of treatment. Although
not usually associated with clinical deterioration,
these variants may induce a severe course in cir-
rhotic or immunosuppressed patients. Lamivudine
is also of benet in patients with HIV/HBV co-
infection, as it is effective against both viruses.
However, such patients have a high likelihood of
developing lamivudine-resistant HBV, which may
be associated with rapidly progressive disease.
Lamivudine is extremely well tolerated, with a
side-effect prole that is no different from placebo.
However, the emergence of lamivudine resistance
may be associated with a are of hepatitis, during
which the patient may develop symptoms of
tiredness, right upper quadrant discomfort and
possibly jaundice and hepatic decompensation.
Patients with lamivudine resistance should con-
tinue to take lamivudine, as its cessation may
result in a severe are of wild-type infection. A
new antiviral agent, adefovir dipivoxil, is extremely
effective in patients with lamivudine resistance,
20
but is currently available only via the TGAs Special
Access Program. It should be prescribed in any
patient with lamivudine resistance who is at risk of
progressive liver disease. In HIV-HBV co-infected
patients with lamivudine resistance, tenovir is
extremely effective at suppressing HBV replication
and improving hepatic function. Other antiviral
agents are currently in clinical trials .
Who should be treated?
In compensated patients with chronic HBV,
antiviral therapy is indicated where there is:
active viral replication (HBeAg+ and/or HBV
DNA positive);
persistently elevated ALT levels;
histological evidence of chronic injury.
The initial aim of treatment is to stop viral repli-
cation as indicated by HBeAg seroconversion
(loss of HBeAg and appearance of anti-HBe) and
loss of HBV DNA. Optimal duration of therapy is
unknown but the current recommendation is to
continue therapy for at least six months after
seroconversion occurs. Once therapy has stopped,
at least 15% of patients will undergo serorever-
sion (i.e. they become HBeAg+ again).
Patients with HBeAg-negative infection
should also be considered for therapy although
the optimal duration of therapy is not known and
patients may need to continue long-term treat-
ment. Patients who are HBeAg-negative with
abnormal LFTs should have an HBV DNA per-
formed. If this is positive, then liver biopsy and
treatment with lamivudine should be discussed.
Liver transplantation in viral hepatitis
Chronic hepatitis C and hepatitis B are the leading
indications for liver transplantation in Australia.
Patients should be referred to a transplant unit
when they develop signs of hepatic decompensa-
tion, such as ascites, encephalopathy, bacterial
infections (particularly spontaneous bacterial
peritonitis), muscle wasting or worsening fatigue.
It is best to try to identify subtle signs of impend-
ing liver failure (Chapters 5 and 7), so that early
referral can be made. Detailed management of
end-stage liver disease is beyond the scope of this
publication but management of some specific
complications is discussed in Chapter 11.
Summary
Chronic hepatitis poses challenges of diagnosis,
general management, selection for treatment, and
care during treatment. It is important that a
patients concerns be addressed by the provision
of information about the disease and access to
counselling and psychosocial support. The prim-
ary care clinician has a vital role in the assessment
and monitoring of patients with chronic viral
hepatitis. Shared care is the preferred model of
care for patients with chronic viral hepatitis and
effective communication between general practi-
tioners, specialists and referral centres is required
for optimal patient management.
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16 Torresi J, Locarnini S. Antiviral chemotherapy for the
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appropriate symptom management, complication
control and palliation.
People in the advanced stages of disease often
have concerns that there will inevitably be severe
pain, loss of independence and loss of dignity. The
aim of palliative care is to improve quality of life
by focusing on the management of symptoms and
the provision of physical, psychological, social
and spiritual support. Good symptom manage-
ment and psychosocial support, embodying the
principles of palliative care, will enable most peo-
ple to maintain independence and enjoy life even
with very advanced disease.
Issues impacting on provision of
palliative care
Clinicians caring for people with HIV/AIDS and
viral hepatitis should be aware of the following
issues which may impact on the patient, his/her
carers and family.
Positive living philosophy
The opportunity should be given to patients to
discuss dying if they are ready to do so. However,
individuals with very real fears of dying may not
want to talk about death, particularly in the era of
optimism associated with modern treatments. In
addition, the cycles of health and ill-health com-
mon in HIV/AIDS may make the identication of
end-stage disease difcult for patients, family and
health professionals. It is quite possible for indi-
viduals to experience improved health after med-
ical interventions associated with palliative care.
This is illustrated in Case study 1.
Fear, stigma and condentiality
Patients may not wish family and/or community
support agencies to be aware of their HIV or
hepatitis status due to fear of discrimination
or rejection. Confidentiality issues may be of
Palliative care
Brian McDonald Director of Palliative Care Medicine, Peninsula Health & Peninsula Hospice, Frankston, Victoria.
Michael Bramwell AIDS Palliative Care Counsellor, HIV/AIDS Unit, Alfred Hospital, Prahran, Victoria.
Norm Roth General Practitioner, Prahran, Victoria.
David Menadue National Association of People With HIV/AIDS, Melbourne, Victoria.
Introduction
The introduction of combination antiretroviral
therapy has improved the prognosis of individuals
with HIV/AIDS and reduced the number of AIDS-
related deaths, although progression to advanced
disease and death still occurs among people with
HIV. In the context of treatment optimism, symp-
tom management and palliative care of people
with advanced HIV/AIDS provides new chal-
lenges, both medical and psychosocial, to health
professionals.
The impact of antiviral therapy on mortality
due to chronic viral hepatitis is as yet unclear. A
substantial number of individuals with cirrhosis
and a number with hepatoma are in need of
Key points
Shared care is crucial to the management of palliative care for
people with advanced and terminal AIDS and viral hepatitis.
The care team may comprise the general practitioner, relevant
specialists, a social worker or counsellor, a palliative care nurse
specialist and clergy. The patient, family members and other
carers may be included in the care team.
Individual palliative needs are best met in the context of
supportive partners and family, who also need consideration.
Support and counselling for family, partners and friends may be
undertaken by the GP or other members of the care team.
Stigma and fear associated with HIV/AIDS and viral hepatitis
may inuence the needs of the patient in relation to
psychosocial support and preparations for death.
The patient should be encouraged to attend to his/her affairs
prior to advanced disease by writing a will and by granting
power of attorney to a trusted individual.
Assessment and management of pain are important features of
palliative care, regardless of a patients use of recreational or
illegal drugs.
Treatment of specic conditions may relieve pain and suffering
and improve quality of life.
11
particular concern in rural and remote areas, and
in some cultural groups. These concerns may
extend to consideration of the certied cause of
death on the death certicate. The clinician may
provide reassurance and assistance with appro-
priate disclosure, and explain the process of certi-
cation of death to assist individuals deal with
these fears.
Sexuality and legal issues
A substantial proportion of people with HIV/
AIDS in the developed world are gay men and
issues of ownership of person and property can
be a source of conict between a gay mans family
and his lover, particularly around the time of
death. All patients should be encouraged to attend
to their affairs prior to advanced disease by
appointing a legal guardian (who is empowered
to make treatment decisions if the patient
becomes incapable of such decisions) and by mak-
ing a will and leaving instructions regarding
funeral and burial/cremation arrangements. Legal
provisions relating to power of attorney exist at
the State and Territory level and referral to
appropriate legal advice may be obtained from
local community groups such as AIDS Councils
(Chapter 14).
Grief and loss issues
Many gay men, drug users and haemophiliacs
with HIV and/or viral hepatitis have been
exposed to multiple losses, with family members,
friends and partners pre-deceasing them.
Cumulative grief responses may manifest in many
ways, such as unexpected and extraordinary reac-
tions to what are seemingly trivial events. This
sense of cumulative loss may impact on the per-
sons ability to cope and may complicate fears
relating to his/her own death. The provision of
psychosocial and counselling support is vital.
Following a death, referral to community pro-
jects, such as the AIDS Memorial Quilt, may be
offered to partners, family members or friends to
assist them to cope with their grief. Referral to a
bereavement counselling service may sometimes
be indicated if risk factors for a complicated
bereavement are present.
Complexity of treatments and disease
People with advanced HIV/AIDS often require
concurrent and continuous treatments for several
AIDS-related conditions with a wide range of
drugs with potential interactions and side-effects.
1
The complexity of advanced HIV disease, due to
coexistent opportunistic infections, malignancies,
adverse events and/or metabolic disorders, may
present a challenge for patients and their families
in understanding disease processes and making
treatment decisions. The question of when to
cease combination antiretroviral therapy is dif-
cult and must be negotiated with the patient.
Some individuals choose to continue with active
treatments until they are very close to death but
these do not preclude treatments to alleviate dis-
tressing symptoms and pain management.
Recreational or illicit drug use
The use of substitution drugs may be required
when a person is admitted to a hospital or pallia-
tive care unit to avoid the effects of withdrawal or
unmasked pain.
2
Because individuals with HCV,
HBV or HIV may have injected drugs, coexistent
or past drug addiction may be an issue in their
palliative care. It is well recognised that under-
treatment for pain, anxiety or psychological stress
has been a feature of the management of individu-
als thought to be addicted to, or potentially
addicted to, alcohol, opiates or benzodiazepines.
The fact that patients have used or continue to
use recreational or illegal drugs should not
preclude the effective use of appropriate anal-
gesics after careful evaluation. High doses may be
required to provide effective pain relief in individ-
uals with a history of opiate usage.
3,4
Acknowl-
edgement of the equal intensity of symptoms and
the right to relief of those symptoms in all patients
are fundamental principles of palliative care.
Consequently, assessment of an increased need for
opiates and effective dosing in tolerant individuals
is appropriate.
CASE STUDY 1
Palliative care: antiretroviral treatment can lead to recovery
Recovery following palliative care
A male patient with severe wasting in the advanced stages of
AIDS is prescribed morphine and midazolam for relief of
discomfort and anxiety. After assessment by a general practitioner
experienced in HIV/AIDS, the patient is admitted to an HIV/AIDS
specic palliative care unit. On discussion, it is evident that he is
keen to pursue life-prolonging treatments including enteral
feeding and antiretroviral combination therapy. Under the joint
management of infectious diseases and palliative care specialists,
his condition improves to the point where he is discharged with
community supports. The man remains well in the community
three years after his time as a palliative care patient.
Cannabis may be used by patients with AIDS
wasting to reduce pain and nausea, and to stimu-
late appetite. The potential benets of marijuana
(e.g. weight gain) should be seen within the con-
text of risk (e.g. bacterial lung infection), particu-
larly among individuals with severe immune sup-
pression.
5
Caring for patients who use illicit drugs may
be complicated by factors such as homelessness,
poverty and mistrust.
Loss of autonomy
A patient may nominate a partner, friend or family
member as his/her advocate or legal guardian in
the event of cognitive impairment or coma. Such a
person may be empowered to make treatment
decisions on behalf of the patient. This may be
particularly appropriate where the patient is alien-
ated from the next-of-kin (Sexuality and legal
issues page 97).
Euthanasia
Some patients with terminal disease consider self-
deliverance in the form of euthanasia or suicide.
6
Euthanasia may be seen as a legitimate answer to
the relentless progress of the disease, loss of inde-
pendence and to the perception of being a burden
to carers, lovers and families.
Acknowledgement of the patients considera-
tion of euthanasia as an option can provide signif-
icant reassurance. Psychiatric evaluation and sup-
port should be routinely offered, as a depressive
illness may warrant treatment and psychological
support.
Doctors and health professionals should be
prepared to discuss requests for euthanasia and
must determine their own responses to such
requests. They may perhaps be prepared to refer
patients to a clinician experienced in euthanasia
issues if uncomfortable with euthanasia them-
selves.
7
Euthanasia is currently illegal in Australia.
A collaborative approach to providing
palliative care
As can be seen from the kinds of issues described
above, people in the terminal phase of HIV/AIDS
or viral hepatitis require access to a continuum of
care encompassing symptom management, respite
care, rehabilitation, terminal care and psychoso-
cial support. Such care can be provided in a range
of settings including the home, an acute medical
unit, an AIDS-specic continuing care or pallia-
tive care unit and in a general hospice or palliative
care in-patient unit.
It is important that this care is provided in
conjunction with an appropriate range of medical
and psychosocial specialists. The primary care
clinician may take an active role in coordinating a
patients care team by liaising with local services
such as support groups, home-care services, and
hospital- or hospice-based social workers, nurses
and specialists.
Palliative care physicians, HIV specialists,
hepatologists and general practitioners may assist
each other with:
assessing the pathophysiology of symptoms;
managing palliative therapeutics;
clinical decision-making in advanced disease;
managing nutritional deciency and uid
retention in end-stage liver disease;
identifying and responding to the
psychological, social and spiritual
components of suffering, and making
appropriate referrals;
breaking bad news to patients and families;
liaising between hospital and home care;
other medical management of the terminal
phase.
11 Palliative care
TABLE 11.1 Opiates and drugs for pain
relief in palliative care
Opiates used in palliative care
Morphine
Diamorphine
Methadone
Hydromorphone
Oxycodone
Fentanyl
Drugs used for neuropathic pain
Methadone
Ketamine
Antidepressants, e.g. amitriptyline, sertraline
Anticonvulsants, e.g. carbamazepine,
gabapentin, sodium valproate
Anti-arrhythmics, e.g. mexiletine, ecainide
Clonidine
Pain management
Pain is common in advanced disease and is often
underestimated and undertreated.
8
Common types
of pain in people with HIV/AIDS are peripheral
neuropathy, headache, abdominal pain, perianal
pain and mouth pain. Side-effects of treatment
may lead to the need for pain relief.
Pain needs to be carefully assessed using
patient self-rating and monitoring tools to isolate
causes and facilitate treatment and intervention.
There is a strong association between psychoso-
cial status and pain intensity, hence the existence
of potentially helpful non-pharmaceutical pain
management strategies such as clinical hypnosis
and emotional and spiritual support.
Drugs for pain management
Analgesic drug use should follow the World
Health Organization (WHO) analgesic ladder
progressing from mild analgesics (e.g. paraceta-
mol) to a combination of mild analgesics with a
weak opioid (e.g. paracetamol plus codeine) or
possibly tramadol before using strong opiates.
Other drugs may be more effective for specic
types of pain including: nonsteroidal anti-inam-
matory drugs; antidepressants (principally tri-
cyclics); anticonvulsant drugs; antispasmodic
drugs; local anaesthetic, and ketamine. Opiates
used in pain management include morphine,
methadone, hydromorphone, oxycodone and fen-
tanyl (Table 11.1). The main indication for substi-
tuting other opiates is where morphine is not well
tolerated. With the exception of methadone for
neuropathic pain, other opiates are unlikely to
provide improved analgesia where morphine has
failed.
Routes of administration include oral, subcu-
taneous, transdermal (fentanyl) and (very rarely)
intrathecal (Case study 2). Advice from specialists
in the eld may be useful for primary care clini-
cians who are unfamiliar with the drug combina-
tions, dosage ranges and methods of administra-
tion which are routine in palliative care.
Neuropathic pain
Painful peripheral neuropathy is common in
HIV/AIDS, occurring in up to 30% of patients,
and post-herpetic neuralgia, while less common,
can be equally disabling.
9
Abolishing pain com-
pletely without unacceptable side-effects may be
extremely difficult but the use of anticonvul-
sants, antidepressants, morphine and other opi-
ates, sometimes in relatively high doses, can
result in signicant improvement.
10
The total daily
dose of morphine may be as much as 3,000 mg
or more.
The use of adjuvant drugs such as tricyclic
antidepressants, anticonvulsants, local anaesthetic
anti-arrhythmics (such as mexiletine) in conjunc-
tion with analgesics can improve management;
however, the response of individual patients is
unpredictable and often disappointing.
11
Methadone or ketamine may provide improved
analgesia (associated with NMDA receptor
antagonist activity) but advice regarding their use
should be sought from specialists in pain manage-
ment or palliative medicine.
12
There is increasing
interest in the role of the anticonvulsants gabapentin
and lamotrigine in neuropathic pain manage-
ment, and intrathecal or epidural morphine is a
recognised treatment option for intractable pain,
but there are no published studies of its use in
patients with HIV/AIDS.
13
Management of other symptoms
AIDS and opportunistic illnesses
Other symptoms in patients with advanced
HIV/AIDS may include debility and weight loss,
fatigue, anorexia, nausea, depression, diarrhoea,
constipation, dyspnoea, cognitive impairment,
dysphagia and neurological decits.
14,15,16
Symptoms due to opportunistic infections
such as candidiasis, herpes simplex, Mycobacterium
avium complex, Pneumocystis carinii pneumo-
nia, toxoplasmosis or cryptococcosis are best
CASE STUDY 2
Palliative care: use of intrathecal morphine
Severe peripheral neuropathy
A patient with advanced HIV disease presents to his GP
complaining of severe peripheral neuropathy. The mans health
improves following commencement of combination antiretroviral
therapy but his peripheral neuropathy persists. After careful
consideration and joint assessment by a palliative medicine
consultant, an infectious diseases physician, a pain management
anaesthetist and a neurologist experienced in the use of
intrathecal morphine, the patient has an intrathecal drug
administration system implanted. Three years later the intrathecal
morphine dose remains stable at 30 mg per 24 hours and his oral
morphine daily dose, which has previously been as high as
2,500 mg, has been reduced to 200 mg daily. His quality of life is
much enhanced.
alleviated by treatment with appropriate antibi-
otics. Some drugs used for symptom management
such as cisapride, non-sedating antihistamines,
midazolam and carbamazepine may have signi-
cant interactions with antiretroviral drugs, partic-
ularly protease inhibitors. Where there is concern
about a particular drug, discussion should be
sought with physicians or pharmacists.
Diarrhoea
Diarrhoea which persists after appropriate assess-
ment and/or treatment by an infectious diseases
physician and gastroenterologist warrants pursuit
of symptomatic management. Dietetics advice
may assist where there appears to be intolerance
to specific foods or supplements. Drugs which
may alleviate symptoms include loperamide,
diphenoxylate, codeine phosphate, opiates and
bulking agents. A trial of a somatostatin analogue
(e.g. octreotide) may be considered.
End-stage liver disease
Treatment is available for several conditions asso-
ciated with end-stage liver disease. For patients
who are not transplant candidates, dramatic
improvements in quality of life may occur follow-
ing dietary intervention or treatment for ascites or
encephalopathy.
Malnutrition is prevalent during end-stage
liver disease, compounding fatigue, wasting and
weakness. Dietary interventions may include
increased calorie intake (e.g. night snacks) and
consumption of proteins and protein supplements
such as Sustagen or branch chain amino acids.
Consultation with a dietitian may be considered.
Fluid retention or ascites is another common
feature of end-stage liver disease that impacts on
nutrition and mobility of the individual.
Management may be dietary (e.g. salt restriction),
medical (e.g. diuretics) or surgical (e.g. paracente-
sis). For intractable ascites, consideration may be
given to insertion of TIPSS (transjugular intrahep-
atic porto-systemic shunt) or to a peritoneo-
venous shunt.
Chronic encephalopathy may improve upon
protein restriction but the laxative lactulose is the
mainstay of management. Long-term prophylac-
tic treatment with the antibiotic noroxacin may
improve or prevent bacterial translocation across
the bowel wall and prevent spontaneous bacterial
peritonitis, as well as improve encephalopathy
and reduce the risk of gastrointestinal bleeding.
Terminal care
Health care professionals, families and other car-
ers may find it difficult to make the transition
from active care to terminal palliative care, even if
the patient is unconscious or heavily sedated.
Discussing the withdrawal of hydration and/or
nutrition, for example, requires great sensitivity
and exibility. The patient may need strong advo-
cacy and the patient and family may need inten-
sive pastoral support throughout this period.
Of paramount importance is the relief of any
pain or other distressing symptoms. Causes of dis-
tressing symptoms should be explored and treated
if appropriate and consistent with treatment
objectives. Investigations should be kept to a min-
imum and only performed if the information
obtained is likely to result in improved symptom
management. Patients often state their acceptance
of drug treatments for relief of symptoms even if
their level of consciousness becomes impaired.
Restlessness or delirium may be a cause of con-
siderable distress to the patient, his/her family and
health care professionals, and it is essential to
relieve such symptoms. Restlessness in most
patients can be well managed with benzodi-
azepines including midazolam, clonazepam and
diazepam but may require large or escalating doses
(Table 11.2). In addition, consideration should be
given to alleviating the causes of restlessness (such
as pain, retention of urine, constipation and faecal
impaction, psychotic symptoms and anxiety).
Patients in the terminal phase of their illness
must have the option of absolute and continuous
relief of distressing symptoms. If there is any
doubt as to the adequacy of symptom manage-
ment, consideration should be given to transfer-
ring the patient to a specialist palliative care unit
or seeking assessment by a palliative medicine
11 Palliative care
TABLE 11.2 Pharmacological treatment of terminal restlessness
Useful drugs Single dose range
clonazepam 0.5 mg to 5 mg
midazolam 2 mg to 15 mg
diazepam 2 mg to 40 mg
haloperidol 2 mg to 20 mg
morphine 2.5 mg to 400 mg
phenobarbitone 100 mg to 400 mg
N.B. Very high doses are necessary only in exceptional circumstances.
The correct dose is the lowest effective dose.
physician or clinical nurse specialist. The use of
regular, preferably continuous, drug administra-
tion will be necessary to avoid uctuation in levels
of symptom management. Ready access to nurs-
ing and medical support is essential.
Counselling (by social workers, clergy or other
appropriately trained health care workers) may
assist partners, families and friends to deal with
their grief at this stage and throughout the nal
weeks of illness.
The proper management of terminal care will
assist in the grieving processes of those who are
left behind. Ongoing support should be available
as necessary throughout the bereavement period,
and those showing signs of abnormal grieving
identied and referred for specialist support.
References
1 Grothe TM. Palliative care for HIV disease. J Palliat
Care 1995;11:48-49.
2 Robb V. Working on the edge: palliative care for
substance users with AIDS. J Palliat Care
1995;11:50-53.
3 Foley FJ, Cook D, Flintoft G, et al. AIDS palliative
care--challenging the palliative paradigm. J Palliat
Care 1995;11:19-22.
4 Kaplan R, Slywka J, Slagl S, et al. A titrated
morphine analgesic regimen comparing substance
users and non-users with AIDS-related pain. J Pain
Symptom Manage 2000;19:265-273.
5 National Institutes of Health Ad Hoc Group of
Experts. Workshop on the Medical Utility of Marijuana:
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6 Meier DE, Emmons CA, Wallenstein S, et al. A
national survey of physician assisted suicide and
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7 Voigt RF. Euthanasia and HIV disease: how can
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8 Breitbart W, Rosenfeld BD, Passik SD, et al. The
under treatment of pain in ambulatory AIDS
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9 Tyor WR, Grifn DE, McArthur JC, et al. Unifying
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Hum Retrovirol 1995;9:379-388.
10 Kaplan R, Conant M, Cundiff D. Sustained-release
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12 Warncke T, Stubhaug A, Jorum E. Ketamine, an
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14 Kelleher P, McKeogh M, Cox S. HIV Infection: the
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1436.
precautions should be implemented universally,
regardless of information or assumptions about
infection status. Transmission based precautions
are further measures required to prevent transmis-
sion when a particular infection, that has a differ-
ent transmission route, is established or strongly
suspected, such as in the case of tuberculosis.
This chapter provides a summary of the
most recent Australian infection control guide-
lines published by the National Health and
Medical Research Council (NHMRC) and
draws on the HIV Guidelines for GPs published
by the Royal Australian College of General
Practitioners, as well as other guidelines.
1,2,3,4
The NHMRC guidelines describe in detail the
practices and procedures necessary to prevent
transmission of blood-borne infections, includ-
ing HIV, HBV and HCV and review of these
guidelines is strongly recommended for individ-
uals implementing infection control procedures.
In addition, compliance with relevant State
and/or Territory guidelines is mandatory
Implementation of standard precautions min-
imises the risk of transmission of blood-borne and
some other infections from health care worker to
patient, from patient to health care worker and
from patient to patient. Some clinicians or health
care workers may feel uncomfortable about
implementing standard precautions, which they
believe may alienate patients. If this is the case, the
health care worker may reassure the patient that
protective procedures and equipment are normal
protocol which exist to protect both patients and
staff. Clinic-based infection control protocols,
recommended by the NHMRC, should be devel-
oped and consulted where staff are not following
appropriate procedures.
Infection control guidelines are relevant in
social and domestic contexts as well as occupa-
tional settings. The clinician should be ready to
answer questions from patients about a clinics
infection control policies and provide advice for
12
Standard precautions and infection control
Nicholas Demediuk General Practitioner, Vice-Chairman of the Dandenong District Division of General Practice,
Dandenong, Victoria.
Steve Wesselingh Director, Burnet Institute, Macfarlane Burnet Institute for Medical Research and Public Health.
Introduction
The potentially infectious nature of all blood and
body substances necessitates the implementation
of infection control practices and policies.
In Australia, infection control guidelines have
been conceptualised, based on the US CDC
model, in terms of standard precautions and
transmission based precautions. Standard precau-
tions ensure a high level of protection against
transmission of blood-borne viruses in the health
care setting and reduce the potential for stigma
and discrimination. They are the minimum level
of infection control required in the treatment and
care of all patients to prevent transmission of
blood-borne infections including HIV, HBV and
HCV, as well as some other infections. Standard
Key points
The potentially infectious nature of all blood and body
substances necessitates the implementation of infection
control practices and policies in the health care setting.
The universal application of standard precautions is the
minimum level of infection control required in the treatment
and care of all patients to prevent transmission of HIV, HBV
and HCV. These include: aseptic technique; barrier protection;
safe disposal systems; correct sterilisation and disinfection
processes, and the appropriate use of instruments and
equipment.
Vaccination is an important infection control strategy for HBV
and HAV; all health care workers should be aware of their
vaccination status and be vaccinated if appropriate.
Clinicians and other health care workers who regularly perform
exposure-prone procedures have a responsibility to be
regularly tested for HIV, HCV and HBV if not immune. Health
care workers who are aware that they are infected with HIV,
HBV or HCV should not perform exposure-prone procedures.
Referral should be made to the most recent NHMRC Infection
Control Guidelines and relevant State and Territory
guidelines.
patients in relation to infection control in their
daily environment.
Transmission
Modes of transmission are outlined briey in Table
12.1 and risk of transmission is discussed in more
detail in Chapter 2. In the health care setting, inci-
dents involving blood-to-blood contact with
infected individuals are associated with a marked
risk of transmission, with the greatest risk being
associated with:
the presence of a large quantity of blood,
indicated by visible contamination;
placement of a needle directly into a vein or
artery or deep injury;
advanced HIV disease, high HIV viral load,
positive HCV PCR, or HBeAg in the source.
In relation to HCV, patient-to-patient transmis-
sion has been associated with endoscopic proce-
dures and a failure to comply with recommended
cleaning and disinfection protocols.
6,7,8,9
Standard precautions
Standard precautions should be applied in the
handling of:
blood (including dried blood);
all other body uids, secretions and
excretions (excluding sweat) regardless of
visible blood;
non-intact skin;
mucous membranes.
Standard precautions, including high levels of
cleanliness, generally provide staff and patients
with adequate protection against blood-borne
viruses. Standard precautions include aseptic tech-
nique, barrier protection, safe disposal systems
and the appropriate use of instruments and equip-
ment, as outlined below.
Hand-cleaning and skin integrity
Hand-cleaning must occur:
before and after each clinical client contact;
before and after eating;
after using the toilet;
before and after use of gloves;
after contact with used equipment;
immediately following contact with body
uids.
Hand jewellery, ideally, should be removed and
hands cleaned with cleaning solution (detergent
with or without disinfectant) and water for 1520
seconds, followed by drying with a single-use towel.
Healthy, unbroken skin provides a valuable barri-
er to infection. Skin breaks should be covered
with a water-resistant occlusive dressing. Alcohol-
based hand rubs can be used in the absence of
appropriate washing facilities.
Gloves
Gloves are a standard precaution and must be
used when:
handling any blood or body uids;
performing venepuncture;
touching mucous membranes;
touching non-intact skin;
handling contaminated sharps;
performing any invasive procedure;
cleaning body uid spills or any equipment
(instruments) or materials (linen) or surface
that may have been contaminated by body
uids.
NHMRC guidelines provide detailed instructions
on appropriate use of sterile and non-sterile
gloves.
Other protective clothing
Additional protective clothing is required in the
following circumstances:
face masks and/or goggles if splashes are
likely;
gown and/or plastic apron if soiling is likely;
footwear should be enclosed and protective
against injury if sharp items are being used.
TABLE 12.1 Mode of transmission and recommended
precautions
5
Disease Mode of transmission Recommended precaution
HAV Contact (oral-faecal route) Standard precautions
Additional precautions for
incontinent patients
HBV Direct contact with Standard precautions
blood or body
substances
HCV Direct contact with Standard precautions
blood or body
substances
HIV Direct contact with Standard precautions
blood or body Additional precautions for
substances complications, e.g. TB
production after vaccination is now viewed as con-
ferring lifelong immunity to the vaccinated,
immune-competent adult.
HAV vaccination is recommended for health
care workers at increased risk of exposure, such as
those working with people with intellectual
impairment, children, or people from rural and
remote indigenous communities. Serology can be
used to assist in the assessment of the need for
HAV vaccination.
No vaccination is available for HIV or HCV.
Testing
The mandatory testing of health care workers
(including general practitioners) for HIV and viral
hepatitis is not warranted, due to the low risk of
transmission if standard precautions are followed.
NHMRC guidelines state that testing should only
be undertaken on the basis of clinical assessment or
where testing is in the interests of patients and
health care workers (e.g. a needle-stick injury).
Clinicians and other health care workers who reg-
ularly perform exposure-prone procedures (Table
12.2) have a responsibility to be regularly tested for
HIV, HCV and HBV if not immune. The provi-
sions of condentiality, privacy and consent for
testing should be applied.
Infected health care workers
Health care workers who are aware that they are
infected with a blood-borne virus should consult
state regulations to determine what restrictions are
placed on their practice. In general it is recom-
mended that they do not perform procedures that
carry a high risk of transmission of the virus from
health care worker to patient. Table 12.2 details
the level of risk associated with specic procedures.
TABLE 12.2 Exposure-prone procedures
10
Risk Procedure
High-risk or exposure- Any submucosal invasion with sharp, hand-held instruments or procedures dealing with
prone procedures sharp pathology/bone spicules, usually in poorly visualised or conned spaces
(e.g. orthopaedic surgery, trauma, internal cavity surgery)
Variable-risk procedures Minor dental procedures (excluding examination), routine dental extractions
Internal/instrument examination/biopsy (e.g. endoscopy, vaginal examination, laparoscopy)
Minor skin surgery
Low-risk procedures Interview consultation, dental examination
Non-invasive examinations or procedures (aural testing, electrocardiograph, abdominal
ultrasound)
Intact skin palpation (gloves not required)
Injections/venepuncture (gloves required)
Needle-stick injury prevention
To minimise the risk of a needle-stick injury,
sharps and clinical waste should be handled care-
fully. Specically:
Minimise handling of sharps and clinical
waste.
Do not bend or recap needles.
Do not remove needles from disposable
syringes.
A safe needle-handling system should be
provided including rigid containers for
disposal. These should be kept out of the
reach of toddlers and small children.
Sharps containers should be at point of use
or in close proximity to work sites to aid easy
and immediate disposal.
Health care workers
Vaccination
Vaccination is an important infection control
strategy for HBV and HAV. The NHMRC and
some State and Territory health departments pro-
vide guidelines on the screening and vaccination
of health care workers. All health care workers
and other staff who may come into contact with
blood or body fluids should be aware of their
HBV vaccination status and be vaccinated if
appropriate. Health care workers who are unable
to demonstrate HBV immunity after supplemen-
tary doses of HBV vaccine may need to be advised
regarding the risks relating to their professional
practice. (Chapter 5 provides a detailed discussion
of exposure management and vaccination regarding
viral hepatitis.) Demonstration of active antibody
12 Standard precautions and infection control
Infection control in the clinic
The NHMRC infection control guidelines pro-
vide detailed information relating to specific
issues, including: routine cleaning; disinfectants
and antiseptics; design and maintenance of health
care premises; management of clinical waste and
linen and reprocessing of instruments and equip-
ment. Specic procedures relating to the ofce
practice and home and community care are
included in the guidelines.
Points that relate to prevention of transmis-
sion of blood-borne viruses include:
All clinical waste such as dressings containing
expressible blood, human matter (excluding
hair, nails, urine and faeces) and blood sharps
must be appropriately packed for transport
and disposal according to local regulations.
Sharps are to be disposed of in yellow, rigid-
walled containers containing the Biological
Hazard label and symbol.
Injecting equipment (including hypodermic
syringes, needles, vials of local anaesthetic
agent, dental local anaesthetic cartridges, den-
tal needles, intravenous lines and giving sets)
must be single-use only. Syringes used to hold
single-use anaesthetic cartridges must be ster-
ilised between patients. Dressings, suture
material, suture needles, scalpels, intracranial
electrodes, pins or needles used for neurosen-
sory testing, spatulas, electric clips and razors
blades must be discarded after single use.
Linen must be managed using standard pre-
cautions. Contaminated linen should have
body substances removed with paper towels
and cold running water, before being washed
in cold or hot water. Drying at high tempera-
ture aids disinfection. Linen which is to be
treated off-site must be packed in labelled,
water-resistant, regulation bags.
Re-usable equipment and instruments should
be re-processed and sterilisation/disinfection
procedures followed in accordance with man-
ufacturers and national guidelines.
Sterile equipment must be used on critical
sites (sterile tissue).
Sterile equipment is generally recommended
for semi-critical sites (intact mucous mem-
brane), except in the case of single-use clean
tongue depressors and vaginal specula, which
are used in procedures unlikely to penetrate
the mucosa.
When steam or dry heat sterilisation is not
suitable, other sterilisation systems such as
ethylene oxide or automated, low-tempera-
ture chemical sterilisation may be used if
acceptable to the instrument manufacturer.
Incident management
Body uid spills (includes blood and
body substances)
Management of spills will depend on the nature
of the spill, likely pathogens, type of surface and
the area involved. A spills kit of cleaning equipment
can be assembled to assist in urgent situations. In
general:
All spills must be dealt with as soon as possible.
In the case of a small spill, wipe the area clean
using a paper towel and then clean with
detergent and warm water. A disposable alco-
hol wipe also may be used. Quarantine areas
where soft furnishings are involved (carpet,
curtains or seating) until dry.
In the case of larger spills mop up with paper
towel or use kitty litter or granular chlorine,
picking up the larger amount with cardboard.
Use cold water if blood is present, to prevent
coagulation.
Injury
If an injury or incident occurs where body uids
come into contact with non-intact skin/ mem-
branes, the following action should be taken:
Wash exposed membrane or injury with
cleaning solution and water (chlorhexidine as
a disinfectant can be used on the skin).
If eyes have been exposed, rinse eyes with tap
water or saline.
If mouth has been exposed, rinse mouth with
water and spit out.
Seek medical advice immediately, as post-
exposure prophylaxis (PEP) treatments are
available for HIV and HBV.
If it is a signicant exposure and if the source
is known, he/she should be approached
regarding consent for HIV antibody, HCV
antibody and HBsAg testing in conjunction
with PEP.
For more information, contact the NSW
Needlestick Injury Hotline 1800 804 823. The
Hotline is a free 24-hour service for health care
and emergency services workers who require
assistance following a needle-stick injury or other
occupational exposure.
In cases of accidental exposure to blood or body
substances, testing procedures and all follow-up
treatment should be fully documented.
3
Post-exposure prophylaxis (PEP)
in the health care setting
Treatments given as soon as possible within 72
hours of exposure may prevent infection with
HIV and HBV. The sooner PEP is administered,
the more likely it is to be effective in preventing
infection. Clinicians should always refer to the
most recent protocols and get appropriate advice,
as this area is constantly changing. Blood should
be taken prior to or shortly after administration
of PEP to check for prior exposure or infection.
Chapters 4 and 5 contain further details.
HIV PEP in the health care setting
HIV PEP is recommended for signicant
percutaneous exposure to blood involving a
high risk of HIV transmission.
HIV PEP is offered (but not actively
recommended) for ocular mucous membrane
or non-intact skin exposure to blood or body
uids.
HIV PEP is not offered for exposure to any
non-bloody urine, saliva or faeces.
2
HBV PEP in the health care setting
If the exposed person is not immune to HBV,
or is of unknown immune status, HBV
immune globulin should be administered
within 72 hours of exposure.
If the exposed person is a non-responder to the
HBV vaccine, HBIG should be given within 72
hours (Chapter 5).
There is currently no PEP for HCV
Legal and ethical issues
Legal liability may occur if inadequate care has
been taken to prevent the transmission of infec-
tion. Regulatory authorities (e.g. environmental
protection) and Commonwealth, State, Territory
and local governments enforce laws and regula-
tions relating to infection control and waste dis-
posal. Their requirements can vary considerably
throughout Australia and such requirements
should take precedence over the general informa-
tion presented in this chapter. Contact State and
Territory health departments and medical and
other professional boards for further details
(Chapter 14). Legal issues are considered in
greater detail in Chapter 13.
Summary
Standard precautions and infection control proce-
dures protect against transmission of blood-borne
viruses including HIV, HBV and HCV in the
health care setting. Regardless of perceived risk,
infection control procedures must be followed in
all clinical settings to minimise the risk of acciden-
tal transmission of these diseases.
References
1 National Health and Medical Research Council
(NHMRC). Infection Control in the Health Care Setting
Guidelines for the prevention of transmission of
infectious diseases Draft. Canberra: Commonwealth
Department of Health and Aged Care; 2001,14 June.
2 Royal Australian College of General Practitioners.
HIV Guidelines for GPs. Melbourne: RACGP;1997.
3 Demediuk N (ed). Sterilisation/Disinfection Guidelines
for General Practice. 3rd edn. Melbourne: RACGP;
2000.
4 NHMRC. National Guidelines for Waste Management
in the Health Industry. Canberra: NHMRC; March
1999.
5 Australian National Council on AIDS and the
National Health and Medical Research Council.
Infection Control in the Health Care Setting. Canberra:
Commonwealth Department of Health and Aged
Care; April 1996:73-74.
6 Crenn P, Gigou M, Passeron J, et al. Patient to
patient transmission of hepatitis C virus during
gastroscopy on neuroteplanalgesia. Gastroent
1988;114:4,A1229.
7 Tennenbaum R, Chochon M, Maisonneuve P, Jean F
and Andrieu J. Hepatitis C after retrograde
cholangiography. Gastroenterol Clin Biol
1993;17:763-764.
8 Cowen AE, Jones D, King B and Rayner T, (eds).
Infection control in endoscopy. Sydney:
Gastroenterological Society of Australia and
Gastroenterological Nurses Society of Australia;
1999.
9 Bronowicki JP, Venard V, Botte C, et al. Patient-to-
patient transmission of hepatitis C virus during
colonoscopy. N Engl J Med 1999;337:237-240.
10 NHMRC. Infection Control in the Health Care Setting
Draft. 2001;14 June:29 (Table 4.1).
12 Standard precautions and infection control
viruses and to encourage effective responses to
treatment and containment. This not only benets
the lives of those infected but also limits the effects
of HIV, HBV and HCV on the wider community.
Public health laws are generally of two types:
punitive or protective. Punitive laws criminalise or
punish certain types of behaviour. There are also
laws that require certain actions to be carried out,
such as notification of prescribed diseases.
Protective laws are those that protect or promote
certain behaviours; for example, anti-discrimina-
tion laws or laws that ensure equal access to health
care. Other than the Quarantine Act 1908 (Cth),
which does not apply to blood-borne viruses, there
is no Commonwealth legislation that deals with
public health. Instead, the States and Territories
have their own legislation. These laws are general-
ly similar in content. In addition to legislation or
statutory laws, the common law plays a signi-
cant role in health law. The common law is law
made by judges as they decide individual cases.
13
Legal responsibilities
Marilyn McMurchie General Practitioner, Darlinghurst, New South Wales.
David Puls Principal Solicitor, HIV/AIDS Legal Centre, Darlinghurst, New South Wales.
Paul Nisselle Health Law Consultant, Melbourne, Victoria.
Anurag Kanwar Research Assistant, HIV/AIDS Legal Centre, Darlinghurst, New South Wales.
Key points
Clinicians are responsible for:
obtaining informed consent before testing for blood-borne
viruses and facilitating informed decision making by patients;
complying with notication requirements;
ensuring the maintenance of condentiality;
providing non-discriminatory care for those infected;
warning a patient, if a doctor or another patient is a potential
hazard to the patient.
Clinicians have a duty of care to their patients to diagnose HIV
and viral hepatitis as well as a duty of care to protect the sexual
partners of these patients from infection.
Clinicians must follow-up patients when test results are positive.
Clinicians have a duty to prevent foreseeable harm.
Full documentation of pre-test and post-test counselling,
recommendations and follow-up is required and may be used
to assist the defence in the event of a legal challenge.
Introduction
The legal responsibilities of clinicians in relation
to blood-borne viral infections are shaped by two
key principles: the protection of public health and
the protection of individual rights. These princi-
ples are embodied in practices such as obtaining
informed consent before testing, complying with
notication requirements, ensuring the mainte-
nance of condentiality and the provision of non-
discriminatory care. In some situations, a clinician
may face conflicting responsibilities and be
required to balance duty to the community at
large with duty to the individual patient. For
example, a breach of the duty of condentiality to
an individual patient may be necessary to protect
the broader community from harm. Generally,
however, respecting the rights of the individual
patient optimises public health outcomes.
This is the principle that was expressed by
Justice Michael Kirby when he described the
AIDS paradox:
My basic thesis is that, paradoxically, the
protection of the human rights of persons at
risk is the most effective way of arresting or
slowing the spread of the virus. This is the
AIDS paradox.
By a paradox, [it is meant that] one of the
most effective laws we can offer to combat
the spread of HIV, which causes AIDS, is
the protection of persons living with AIDS,
and those about them, from discrimination.
This is a paradox because the community
expects laws to protect the uninfected from
the infected.
1
The law can, as part of an integrated approach
involving treatment, education, patient advocacy,
appropriate media coverage and changing com-
munity understanding, provide a supportive envi-
ronment to minimise the spread of blood-borne
Testing
Given that the consequences for the patient of
either being tested or not being tested for a blood-
borne virus may be considerable, it is wrong to
treat tests for such pathogens as standard or
routine, if that term implies the lack of a need for
informed consent specic to each test. Principles
of medical ethics, as well as laws, require that all
medical procedures, including testing for HIV,
HBV and HCV, be carried out only after the
patient has provided informed consent for the
procedure. Consent is valid only if it is given with-
out coercion by an informed and competent
patient. In some jurisdictions and with respect to
some diseases (most notably HIV), these obliga-
tions are made explicit by statute. The provision
of treatment without consent constitutes a tres-
pass. However, where consent has been obtained
in broad terms that is, the patient has been
informed about the nature and general purpose of
the proposed procedure, but there was a failure to
disclose material risks, there is no trespass but
there is negligence. Whilst commonly referred to
as failure of informed consent, this is more prop-
erly described as disclosure negligence.
In addition to the statutory obligations imposed
on clinicians that either specically or generally
impact on the management of patients infected
with blood-borne viruses [most specically Section
7 (s.7) HIV/AIDS Preventive Measures Act 1993
(Tas)], there also are common law obligations.
The doctor must provide sufcient information
to ensure the patients right of self-determination
has been satised. The concept of informed con-
sent is too narrow when informed decision mak-
ing is required. A patient may decide to accept or
reject the doctors advice. A decision to refuse the
doctors advice must be seen to be as fully
informed as one to accept the advice, both ethi-
cally and as a matter of law. When a clinician
advises testing for HIV, HBV or HCV, the patient
must be provided with sufcient information, in a
form that he/she is capable of understanding, to
enable the patient to make an informed decision
whether or not to be tested. The doctor has a duty
to provide information to each individual patient
in a style and manner such that that particular
patient is able to absorb it as knowledge.
Information must be fairly balanced; that is, both
the benets of testing and the possible negative
sequelae must be discussed. Both positive framing
(an overemphasis on benefits) and negative
framing (an overemphasis on risks) can unduly
inuence the patients decision.
2
The doctor has
no duty to the patient to ensure that he or she
makes a wise decision. Indeed, it is a fundamen-
tal principle of the patients right of self-determi-
nation and bodily integrity that he/she makes
his/her own decisions, regardless of whether a
third party perceives the decision to be wise or
not. Detailed documentation of pre-test and post-
test counselling (Chapter 8) is recommended as
evidence of proper information disclosure in case
of legal challenge.
Based on the High Courts decision in Rogers
v Whitaker
3
, in which a woman undergoing eye
surgery was not warned of a rare side-effect of
surgery that left her almost totally blind, the fol-
lowing tests apply to information disclosure.
These tests are additive, not alternative.
The Reasonable Patient test
All the information that any reasonable person
would think material or relevant to making a
decision regarding testing must be provided.
The Reasonable Doctor test
The additional information that any reasonable
doctor would or should add, due to its relevance
to the particular patient, must be provided. Any
reasonable doctor would know that a sex worker,
for example, is a special case in relation to HIV
testing, as is a patient who is already immuno-
compromised.
The Individual Patient test
Any additional information that the patient
requests must be provided. Additional informa-
tion needs to be solicited by open-ended questions
such as Is there anything else you would like to
know?
These legal tests also apply to the treatment
and care of patients infected with blood-borne
viruses. The High Court has recently reconsidered
and upheld these principles in Rosenberg v Percival.
4
Condentiality
There is a distinction between different types of
disclosure in a medical setting. There is disclosure
of information where public health issues are con-
cerned (where condentiality is usually protected)
and general disclosure (where condentiality is
often not protected).
In each State and Territory, HIV, hepatitis B
and hepatitis C are notifiable diseases and
13 Legal responsibilities
clinicians are required to provide the relevant
health authorities with information regarding
these infections. In some legislation and regula-
tions, HIV/AIDS attracts stricter guidelines relat-
ing to notification and disclosure than those
established for other infectious diseases such as
hepatitis B and hepatitis C. In New South Wales,
South Australia, Victoria and Tasmania, notica-
tion of cases of HIV/AIDS must be in coded form,
ensuring anonymity and condentiality. Coded
notification of HIV/AIDS may also occur in
Queensland.
The second type of disclosure or breach occurs
where the health care worker discloses medical or
other information (e.g. positive HIV status) about
a person in addition to the persons name, address
or other identifying characteristics. The basic
principle is that a health care worker, like any per-
son, has a duty not to breach condentiality when
he/she comes into possession of information that
is condential. In some circumstances, there is an
implied waiver of the right to have the matter kept
condential. For example, matters directly related
to the immediate health care of the patient are
likely to be communicated to others directly
involved in the provision of that health care. The
implied waiver applies only to information trans-
ferred in the patients interest required directly for
that episode of care. Passing information for the
purpose of protecting other health care workers
may not satisfy this test.
If condentiality is breached, the patient may
sue for damages and/or complain to the local
medical disciplinary authority, health complaints
authority or, in some jurisdictions, the local privacy
authority. For example, if a health care worker
disclosed someones HCV status in a small coun-
try town and that person was forced to move, the
patient may have a successful action for damages
for removal costs as well as for pain and suffering,
loss of enjoyment of life and emotional stress. A
concurrent complaint to that health care workers
registration authority may lead to disciplinary
sanctions.
There have also been legislative attempts to dis-
courage such disclosure. There are general obliga-
tions in New South Wales, Victoria, Queensland
and South Australia stating that certain categories
of health care professionals (primarily those
employed by public hospitals) are required not to
disclose medical information obtained during
course of their duties [s.22 Health Administration
Act 1982 (NSW); s.141 Health Services Act 1988
(Vic); s.49 Health Act 1937 (QLD); and s.64 South
Australian Health Commission Act 1976 (SA)].
A breach of condentiality in New South Wales,
Tasmania and the Australian Capital Territory is a
criminal offence [s.17 Public Health Act 1991
(NSW); s.19 HIV/AIDS Preventive Measures Act
1993 (Tas); and s.110 Public Health Act 1995
(ACT)]. The duty of condentiality in New South
Wales extends to any service provider not just
health workers (s.17). However, s.17 (3) of the
Public Health Act 1991 (NSW) provides that
information about a persons HIV status can be
disclosed to a person who is involved in the provi-
sion of care to, or treatment or counselling of the
other person if the information is required in con-
nection with providing such care, treatment or
counselling... It should be noted that s.17 pro-
tects patients condentiality regarding informa-
tion about HIV and AIDS but not viral hepatitis.
The duty of condentiality in Tasmania is con-
ned to HIV testing and there is a list of circum-
stances in which the duty does not apply.
Victorian legislation imposes a criminal penalty
on health professionals if they do not have an
appropriate system for protecting the privacy of
people tested for HIV (Health Act 1958 (Vic)
s.128). In South Australia, s.42 of the Public and
Environmental Health Act 1987 (SA) protects con-
dentiality by imposing a ne for breaches of con-
dentiality. Under Queensland legislation any per-
son, body corporate and/or association of persons
may suffer penalties for a breach of condentiality.
In general, clinicians have both ethical and
legal obligations to establish and maintain sys-
tems for protecting the condentiality of informa-
tion about their patients. This is not just a matter
of self-protection from the risk of litigation, it also
builds the condence of patients and potential
patients in the integrity of clinicians, their institu-
tions and their staff.
Privacy
In addition to longstanding common law and ethi-
cal and statutory condentiality obligations, health
care workers must now abide by a raft of privacy
laws that have been enacted by the Commonwealth
Government and by a number of State
Governments. Those laws recognise that health
information privacy is perhaps the most sensitive
information of all and deserves special treatment
and protection. The privacy laws will require health
care workers and the organisations that employ
them to undertake and to be seen to have undertak-
en, a range of practices aimed at enhancing and
respecting condentiality, privacy, security, open-
ness and transparency. The relevant legislation
affecting the private sector throughout Australia is
the Privacy Amendment (Private Sector) Act 2000
(Cth). It applies to all private sector health
providers and came into effect on 21 December
2001. Some States have sought to address health
privacy through health-specic privacy legislation,
which extends to both the public and the private
sectors. For example, the Victorian Government
enacted the Health Records Act (2001) which came
into force on 1 July 2002.
Notication
In all States and Territories, hepatitis B, hepatitis
C and HIV/AIDS are notiable conditions. This
requires clinicians to notify the relevant health
authorities when a new case is diagnosed.
Legislation has attempted to strike a balance
between preserving the privacy of the individual
and the greater public interest in curbing the
spread of notiable conditions.
New South Wales, Queensland, Northern
Territory, South Australia, Tasmania and the
Australian Capital Territory require clinicians to
report any incidence of a notiable disease as soon
as is practical [s.14(1) Public Health Act (NSW);
s.32A(1) Health Act (QLD); s.6 Notifiable
Diseases Act 1981 (NT); s.102(3) Public Health
Act (ACT); and s.30 Public and Environmental
Health Act (SA)]. The denition of what is practi-
cal will depend on the facts of the specic case. In
most States and Territories, pathology laborato-
ries may also undertake notication of notiable
diseases.
Under Western Australian legislation the
obligation of notication rests with both the clini-
cian and the occupier of the house where a person
is found to be suffering from an infectious disease
[s.276 Health Act 1911]. In contrast, Victoria
requires clinicians to notify the relevant health
authorities immediately by telephone and then
send written conrmation within seven days of
conrmation of original diagnosis [Schedule 2,
Health (Infectious Diseases) Regulations 1990].
Referral to State and Territory health departments
is recommended for full details of notification
requirements (Chapter 14).
Non-discrimination
The Commonwealth and all States and Territories
have legislation making discrimination illegal on
the grounds of disability or perceived disability,
impairment and handicap.
In each State or Territory where legislation
exists, except South Australia, HIV and hepatitis C
status falls within the denition of disability in the
anti-discrimination legislation. Thus, it is illegal to
discriminate on the basis of a persons actual or per-
ceived HIV or hepatitis status. In other words, it is
illegal to discriminate against someone whom a
person believes to be HIV-infected, whether or not
they are actually HIV-infected. In South Australia,
the law prohibits discrimination on the ground of
impairment. Impairment is dened in such a way
that it covers AIDS and symptomatic (but not
asymptomatic) HIV infection.
Historically, the greatest source of complaint
about HIV discrimination has been health care
settings. Hepatitis B and hepatitis C pose similar
issues. The most common type of unlawful dis-
crimination relevant to blood-borne viruses has
been on the ground of an attribute considered by
the health care worker to be a risk factor for dis-
ease, such as homosexuality (or perceived homo-
sexuality). In this context, it should be noted that
recent case law recognises drug dependency as a
disability that is protected from unlawful discrim-
ination.
The denition of discrimination varies in the
different legislation. Generally, discrimination on
the ground of disability occurs when one person
treats another person less fairly than he/she would
someone without that disability, or harasses
another person because of his/her disability.
3,5
Likewise, discrimination on the ground of homo-
sexuality (or, in New South Wales, of being a
transgender person) occurs when, on that ground,
a person is treated less fairly than a person with-
out the attribute of homosexuality (or being
transgender).
In situations where a persons disability poses
real issues, such as a health risk, the policy of anti-
discrimination statutes is to encourage employers
and service providers to take reasonable steps to
accommodate the persons disability. This can be
done by adopting recognised measures for infec-
tion control, by making reasonable adjustments in
practice, in scheduling and so on. A failure to rea-
sonably accommodate a persons disability will be
taken into account in deciding whether or not an
act of discrimination was unlawful.
New South Wales differs from the other States
and Territories, as it is the only state that outlaws
vilification on the grounds of HIV/AIDS, of
homosexuality and of being a transgender person.
Vilication is dened as doing anything publicly
that could encourage or incite hatred, contempt
or severe ridicule.
Infected health care workers
The requirements for information disclosure also
apply to the ethical and legal obligations of health
professionals infected with blood-borne viruses. If
a doctor or another patient is, for any reason, a
potential hazard to a patient, the patient has the
legal right to be warned of that hazard. This is
because the Rogers v Whitaker High Court judge-
ment underscored the patients right to be
informed of all material risks. Even a small risk
of contracting HIV, HBV or HCV infection from
a health care worker or another patient may be
perceived as material. A health care worker
infected with a blood-borne virus has a duty to
assess whether, in the context of his or her prac-
tice, there is a material risk that HIV, HBV or
HCV infection could be transmitted to a patient.
If there is, and the health care worker continues in
that practice, then there are both legal and ethical
burdens requiring disclosure of that risk.
In this context, the health care worker will
take into account factors such as:
the magnitude of the harm that transmission
would cause;
the degree of risk of transmission involved in
the procedure or other contact;
the infection control procedures to be adopt-
ed or in place;
the advice received from a clinician skilled in
such assessments.
Risk of transmission in the health care setting is
discussed in Chapter 12. Infected health care
workers can consult relevant professional or pub-
lic health authorities for clarication of risk and
relation to professional practice.
Diagnosis malpractice
A doctors duty of care to diagnose HIV and
chronic viral infections applies to patients and
their sexual partners, following the judgement in
BT v Oei (Case study 1). In this case, the doctor
was found negligent in not advising testing for
HIV and the court agreed that this negligence led
to BT becoming HIV infected.
Another form of diagnosis malpractice is the
failure to follow-up a positive test result. In Kite v
Malycha
7
, Justice Perry found a surgeon negligent
for not informing a patient that a ne-needle aspi-
ration biopsy of a breast lump showed cancer cells.
The surgeon did not have a system for detecting
that the patient had not received the test result. Part
of his defence was that the patient did not follow
his advice to phone for the result in a few days and
return for review in a few weeks. However, Justice
Perry stated in his judgement that: [Mrs Kite] was
entitled to assume that if the outcome of the testing
of the biopsy gave cause for concern, she would be
informed. Thus he rejected an argument that Mrs
Kite contributed to or caused her own damage
through her failure to carry out the surgeons
advice regarding follow-up.
Because testing for HIV antibody status is
largely anonymous (that is, the blood sample is
often sent without patient identication but with
a code assigned by the referring doctor), the
CASE STUDY 1
Diagnosis malpractice, negligence and duty of care
Failure to recommend HIV testing
In a NSW case, BT v Oei
6
, the defendant doctor was found to
have a duty of care to a patients sexual partner, even though the
partner was not herself a patient of the doctor. The case involved
a man (AT) who reported a u-like illness in late 1991 and
developed acute hepatitis B and a urinary tract infection in early
1992. A woman called BT subsequently formed a sexual
relationship with AT and became infected with HIV.
Despite Dr Oeis testimony to the contrary, the court found that
Dr Oei did not recommend HIV testing. As a result, AT was
unaware of his HIV status and subsequently passed the virus to
BT. BT sued the doctor claiming that his failure to diagnose ATs
HIV infection was negligent. BT asserted, and the court agreed,
that the doctor should have advised AT to have a HIV test when
AT rst presented. The doctor certainly owed a duty of care to AT.
The question asked of the court, and answered in the afrmative,
was whether he also owed a duty of care of BT.
Justice Bell, in nding for BT, took note of the provisions of the
Public Health Act 1991 (NSW), which requires a doctor who
believes a patient is HIV-infected to inform that patient of the
danger he/she poses to others and to advise the measures he/she
should take to protect others from cross-infection. Justice Bell
found the doctor negligent in not suspecting the presence of HIV
infection. If he had suspected HIV infection and had followed the
dictates of the Public Health Act then, on the balance of
probabilities, ATs HIV status would have been diagnosed early
enough for him to have practised safe sex with BT and BT, again
on the balance of probabilities, would not have contracted HIV
infection. Thus, Dr Oei was found negligent and his negligence
was found to have caused BTs damage.
judgement in Kite v Malycha makes it probable
that a doctor who does not have a system to check
that results are received for all requested/referred
tests and that those results are communicated to
the relevant patient, will be held to be negligent.
The BT v Oei judgement would suggest that
the liability in negligence will extend both to the
patient and to anyone else unwittingly infected by
that patient in the belief that no communication
from the doctor meant that the test must have
been negative. If Justice Perrys judgement in the
Supreme Court of South Australia is supported in
other State jurisdictions (or by the High Court of
Australia), then patients referred for HIV anti-
body testing will be seen to be legally entitled to
assume that no news is good news. That is, if the
doctor does not contact them about the test, it
must have been negative.
Another recent NSW judgement (PD v Dr
Nicholas Harvey & 1 Ors [2003] NSWSC 487),
handed down in June 2003, reinforces this point.
A couple attended a GP together for pre-marital
counselling and STD screening. The man was
found to be HIV positive. When he was given the
result, he was referred to a specialist HIV clinic.
When the woman rang, having ascertained that
she was HIV negative, she asked about the mans
result. She was told she could not be given the
mans result without his consent. It transpired
later that he told her that his result was negative,
they had unprotected intercourse, and she became
infected with HIV. She sued the doctors involved.
In his judgement Cripps AJ supported the doc-
tors observance of their duty not to disclose the
mans result to the woman without his consent.
However, having ascertained that the man had
not told the woman his result, and that he did not
attend the specialist clinic, the judge found that
the GPs were in breach of their statutory duty
(under NSWs Public Health Act 1991) to notify
the Director-General of Health that an HIV posi-
tive patient was placing another individual at risk.
Under that Act the Health Department had legis-
lated power to intervene. Further, the judge found
that the pre-test counselling at the original joint
consultation was negligently provided in that it
did not meet the standard required under guide-
lines issued by the NSW Department of Health.
Many patients are reluctant for the doctor to
ring their home or workplace, some patients
instruct their doctors not to ring under any cir-
cumstances, and other patients attend giving a
false name and false contact details. In such situa-
tions, the doctor is unable to initiate passing the
result to the patient but relevant public health
authorities must, of course, be informed of posi-
tive test results regarding notiable diseases. At
the same time, the clinician can report that the
patient had not sought the result and could not be
contacted. It would then be a matter for the pub-
lic health authority to nd the patient.
Prevention of foreseeable harm
A clinician could be found liable in negligence to a
third party if he/she knows that an HIV-infected
patient is recklessly putting others at risk, but
does not warn that third party or the relevant
health authorities.
Though there is doubt as to its relevance to
Australian law, the 1976 Californian case
Tarasoff v The Regents of the University of
California,
8
centred on this point. A psychologist
was found to have been negligent in not warning
the ex-girlfriend of a patient that the patient had
expressed to the psychologist, an intent to kill the
ex-girlfriend. The patient subsequently did mur-
der the girl and her parents sued successfully for
failure to warn.
A similar case could succeed in relation to a
patient with a blood-borne virus, either where a
specic individual is placed at risk (for example,
the much-debated scenario in which an HIV-
infected man refuses to tell his wife his HIV status
and refuses to practise safe sex with her a situa-
tion very similar to that is PD v Harvey) or where
the community at large is placed at risk (for exam-
ple, an HIV-infected sex worker who admits to
providing sexual services without a condom to
attract higher fees). In the latter case, if a doctor
did not report those circumstances to the health
authorities, a person who later contracted HIV
infection from that sex worker might well bring a
successful action in negligence against the doctor.
In the former case, even if the patients spouse is
not a patient of that doctor, the duty to prevent
foreseeable harm might require the doctor to
ensure the spouse is protected from the risk of
harm, even if specically instructed by the patient
not to contact the spouse. The doctors duty of con-
dentiality to the patient can often be reconciled
with the duty to prevent foreseeable harm by tak-
ing advantage of facilities offered by health
departments for dealing with such cases the
point made by Cripps AJ in PD v Harvey. In cases
where experienced sexual health counsellors are
available, it may often be better to involve them in
the task of reducing the risk of harm of transmission to a
patients partner.
In general, it is preferable for the doctor to report
directly to public health authorities rather than attempt
to make contact with the person thought to be at risk.
See Chapter 14 for contact information for services
able to advise on legal issues.
References
1 Law Discrimination and Human Rights Facing up to the AIDS
paradox. Third International Conference on AIDS in Asia
and the Pacic. Chiang Mai, Thailand; 1995.
2 McDonalds market a new range of fast foods under the
slogan 97% fat free. Thats positive framing. The converse
would be to label them 3% fat.
3 Rogers v Whitaker (1992) 175 CLR 479; 109 ALR 625 (HCA).
4 Rosenberg v Percival (2001) 8 HCA 18.
5 New South Wales Anti Discrimination Act (1991) s.49B.
Queensland Anti Discrimination Act (1991) s.10.
South Australian Equal Opportunity Act (1984) s.66.
Victorian Equal Opportunity Act (1995) s.7.
Tasmanian Anti Discrimination Act (1998) s.14.
West Australian Equal Opportunity Act (1984) s.66A.
Australian Capital Territory Discrimination Act (1991) s.8.
Northern Territory Anti Discrimination Act (1992) s.20.
6 BT v Oei [1999] NSWSC 1082.
7 Kite v Malycha (1998) 71 SASR 321.
8 Tarasoff v The Regents of the University of California 1976 CA
131 Cal Rptr 14, 551 p2d 334 CA Supreme Court.
Contact and referral information
Phone number Website
GENERAL CONTACTS
Australasian Society for HIV Medicine (ASHM) 02 9368 2700 www.ashm.org.au
Commonwealth Department of Health and Ageing 02 6289 1555 www.health.gov.au/
(Population Health Division) www.health.gov.au/pubhlth/
Ministry of Health New Zealand 0011 64 496 2000 www.moh.govt.nz/moh.nsf
National Health and Medical Research Council (NHMRC) 02 6289 9184 www.nhmrc.gov.au
National Drug & Alcohol Research Centre (NDARC) 02 9398 9333 www.med.unsw.edu.au/ndarc/
STATE/TERRITORY HEALTH DEPARTMENTS
ACT 02 6205 5111 www.health.act.gov.au/dept.html SA 08 8226 8800 www.health.sa.gov.au/
NSW 02 9391 9000 www.health.nsw.gov.au/ TAS 03 6233 3185 www.dhhs.tas.gov.au/
NT 08 8999 2400 www.nt.gov.au/ VIC 03 9616 7777 www.dhs.vic.gov.au/
QLD 07 4920 6953 http://www.health.qld.gov.au/ WA 08 9222 4222 www.health.wa.gov.au/
Many useful NSW health department circulars can be found at: http://www.health.nsw.gov.au/fcsd/rmc/cib
PROFESSIONAL BODIES
Australasian Society for HIV Medicine (ASHM) 02 9368 2700 www.ashm.org.au/
Australian College of Ambulance Professionals www.acap.org.au/
Australian College of Rural and Remote Medicine 07 3352 8600 www.acrrm.org.au
Australasian College of Sexual Health Physicians (ACSHP) 02 9382 7457 www.acshp.org.au/
Australian Dental Association 02 9906 4412 www.ada.org.au/
Australian Division of General Practitioners 02 6251 3380 www.adgp.org.au/
Dietitians Association of Australia 02 6282 9555 www.daa.asn.au/
Gastroenterological Society of Australia (GESA) 02 9256 5454 www.gesa.org.au/
Hepatology Nurses Group 02 9828 5906
International Association of Physicians in AIDS Care (IAPAC) 312 759 4930 www.iapac.org/
Royal Australian College of General Practitioners (RACGP) 03 9214 1414 www.racgp.org.au/index.htm
Royal Australian College of Physicians (RACP) 02 9256 5444 www.racp.edu.au/
Royal College of Nursing Australia 02 6282 5633 www.rcna.org.au/
Royal College of Pathologists of Australasia 02 8356 5858 www.rcpa.edu.au/
Social Workers in AIDS (SWAIDS) 02 9843 3124
The following list provides phone numbers and websites (if applicable) for a range of national and state services that will be useful to
both clinicians and patients. Please also consult the ASHM Directory (available from the ASHM ofce and online at www.ashm.org.au)
for further details of HIV/AIDS and hepatitis C specialists and services to assist you in making appropriate referrals.
14
MEDICAL AND PATHOLOGY SERVICES
Australian Infection Control Association 0414 422307 www.aica.org.au/
Australian Red Cross Blood Service (to connect to local blood banks) 13 14 95 www.giveblood.redcross.org.au
National Serology Reference Laboratory 03 9418 1111 www.nrl.gov.au/
Victorian Infectious Diseases Reference Laboratory 03 9342 2636 www.vidrl.org.au
(This website has an excellent links page for infectious diseases/serology information)
HIV/AIDS CONTACTS
National
Australian Federation of AIDS Organisations (AFAO) 02 9281 1999 www.afao.org.au/
Australian Research Centre in Sex, Health & Society 03 9285 5382 www.latrobe.edu.au/www/arcshs/
(collaborating with the NCHSR)
National Association of People Living With HIV/AIDS (NAPWA) 02 9281 2511 www.napwa.org.au
National Centre in HIV Epidemiology and Clinical Research 02 9332 4648 www.med.unsw.edu.au/nchecr/
National Centre in HIV Virology Research 02 9845 9005 www.hiv.edu.au/
National Centre in HIV Social Research (NCHSR) 02 9385 6776 www.arts.unsw.edu.au/nchsr/
New Zealand AIDS Foundation 0011 64 9303 3124 www.nzaf.org.nz
AIDS Councils
AIDS Action Council of the ACT 02 6257 2855 www.aidsaction.org.au/
AIDS Council of NSW 02 9206 2000 www.acon.org.au/
Northern Territory AIDS Council 08 8941 1711 www.octa4.net.au/ntac/
Queensland AIDS Council 07 3017 1777 www.quac.org.au
AIDS Council of South Australia 08 8362 1611 www.aidscouncil.org.au/
Tasmanian Council on AIDS and Related Diseases (TasCAHRD) 03 6234 1242 www.tascahrd.org.au
Victorian AIDS Council/Gay Mens Health Centre (VAC/GMHC) 03 9865 6700 www.vicaids.asn.au/
Western Australian AIDS Council 08 9482 0000 www.waaids.com
People Living with HIV/AIDS (PLWHA) groups
Body Positive Inc (New Zealand) 0011 64 9309 3989 www.bodypositive.org.nz
PLWHA ACT 02 6257 4985 http://www.aidsaction.org.au/plwha/
PLWHA NSW 02 9361 6011 http://www.plwha.org.au/
PLWHA NT 08 8941 1711 info@ntac.org.au
Positive People (QLD) 07 3844 1990
PLWHA South Australia 08 8293 3700 http://www.hivsa.org.au/
Positive People Tasmania 03 6234 1242 www.tascahrd.org.au
PLWHA Vic 03 9865 6772 http://www.gaynet.com.au/plwha/
WA see Western Australian AIDS Council 08 9482 0000 www.waaids.com
Positive women
AIDS Council of NSW Positive Womens Support 02 9206 2012 www.acon.org.au/
Information on Children, Parenting and Pregnancy 02 9382 2222 www.health.nsw.gov.au/publichealth
Paediatric AIDS Unit, Sydney Childrens Hospital
Ladies Into Positive Support (LIPS) (QLD) 07 3846 3939 www.quac.org.au/qpp
Positive Women Victoria 03 9276 6918 www.positivewomen.org.au
Womens Health Statewide HIV/AIDS Project (SA) 08 8267 5366
continued >
14 Contact and referral information
Positive heterosexuals
HIV Positive Heterosexuals (NSW) Freecall 1800 812 404 02 9515 3095
Straight Arrows (VIC) 03 9267 3792 http://www.straightarrows.org.au
Services for young people
ACON Fun and Esteem 02 9206 2077
Second Storey Youth Health Service (SA) 08 8326 6053
Toehold in Queensland 07 3844 1990
VAC Young and Gay 03 9865 6700 www.vicaids
There is also a useful directory of Australia-wide services for people living with HIV/AIDS at: www.hivaids.webcentral.com.au/text/dir.html
Other community contacts
AIDS Dementia and HIV Psychiatry Service (ADAHAPS) (NSW) 02 9339 2078 www.digitalmetworkmanagement.com/adahps/
Australian IV League (AIVL) 02 6279 1600 www.aivl.org.au
Bobby Goldsmith Foundation 02 9283 8666 www.bgf.org.au/
Haemophilia Foundation of Australia 03 9885 7800 www.haemophilia.org.au
Transfusion-related AIDS (TRAIDS): Medically Acquired Hepatitis C 02 9843 3143
and HIV, Counselling, Support and Advocacy Centre
HEPATITIS CONTACTS
National organisations
Australian Hepatitis Council (ACH) 02 6232 4257 www.hepatitisaustralia.com/
Hepatitis C Councils and support networks
ACT 02 6253 9999 www.acthepc.org SA 08 8362 8443 www.hepccouncilsa.asn.au
NSW 02 9332 1599 www.hepatitisc.org.au TAS 03 6234 1242
NT 08 8941 1711 www.ntac.org.au VIC 03 9380 4644 www.hepcvic.org.au
QLD 07 3229 3767 www.powerup.com.au/~hepcq WA 08 9328 8538 www.users.highway1.com.au/~hepccwa/
Alcohol and Drug Information Services (ADIS)
These are 24-hour services unless otherwise specied:
ACT 02 6205 4545
NSW 02 9361 8000
NT 08 8981 8030 1800 629 683 8.30am to 4.30pm Monday to Friday
QLD 07 3236 2414 1800 177 833
SA 08 8363 8618
TAS 03 62336722 1800 811 994
VIC 03 9416 1818 1800 136 385 131570 (Drug Info)
WA 08 9442 5000 1800 198 024
NEEDLE AND SYRINGE PROGRAMS / METHADONE PROGRAMS
Information on these services can be obtained from either ADIS (page 115) or the following drug user groups:
ACT Canberra Injectors Network (CIN) 02 6262 5299
NSW New South Wales Users and AIDS (NUAA) 02 9557 1476 1800 644 413
NT (Darwin) Health for Injectors in the NT (TUF) 08 8941 1711 www.ntahc.org.au
(Alice Springs) Central Australia Injectors Network (CAIN) 08 8953 6503
QLD Queensland Intravenous AIDS (QuIVAA) 07 3252 5390 1800 172 076
SA South Australian Voice for IV (SAVIVE) 08 8362 9299
TAS Tasmanian Users Health and Support (TUHSL) 03 6234 1242 www.tascahrd.org.au
VIC Victorian Drug Users Group (VIVAIDS) 03 9419 3633
WA WA Substance Users Assocation (WASUA) 08 9227 7866
A useful website with links to many services can be found at the Alcohol and Drug Information Network (ADIN): http://www.adin.com.au/
EDUCATION AND TRAINING CONTACTS
AIDS Dementia and HIV Psychiatry Service (ADAHP) 02 8382 1810 www.health.nsw.gov.au/adahps
Albion Street Centre 02 9332 9600 www.sesahs.nsw.gov.au/albionstcentre/
Australasian College of Sexual Health Physicians (ACSHP) 02 9382 7587 www.acshp.org.au/
Australasian Society for HIV Medicine (ASHM) 02 9368 2700 www.ashm.org.au/
HIV Continuing Medical Education Project
Australian Centre for Health Promotion 02 9351 5129 www.achp.health.usyd.edu.au/
Australian Research Centre in Sex, Health and Society 03 9285 5382 www.latrobe.edu.au/www/arcshs/
Centre for Community Welfare Training (CCWT) 02 9281 8822 www.acwa.asn.au/ccwt/
FPA Health (formerly Family Planning Australia) 02 6230 5255 www.fpa.net.au
NSW Health Workforce Development Program/ 02 9368 2724 www.wdp.nsw.gov.au/
Hepatitis C Workforce Development Project
Royal Australian College of General Practitioners (RACGP) 03 9214 1414 www.racgp.org.au/
Royal College of Nursing Australia 02 6282 5633 www.rcna.org.au/
See also State and Territory Health Departments listed above.
LEGAL SERVICES
Anti-discrimination bodies
ACT Human Rights Ofce 02 6207 0576 http://www.hro.act.gov.au
NSW Anti-Discrimination Board 02 9268 5555 www.lawlink.nsw.gov.au
NT Anti-Discrimination Commission 08 8981 3813 www.adc.nt.gov.au
QLD Anti-Discrimination Commission 07 3247 0960 www.adcq.qld.gov.au
SA Equal Opportunity Commission 1800 188 163 www.eoc.sa.gov.au
TAS Anti-Discrimination Commission 03 6233 4841
VIC Equal Opportunity Commission 03 9281 7110 www.home.vicenet.net.au
WA Equal Opportunity Commission 08 9264 1930 www.equalopportunity.wa.gov.au
HIV/AIDS Legal Centre (NSW) 02 9206 2060 www.halc.org.au
Human Rights and Equal Opportunity Commission 02 9284 9600 www.hreoc.gov.au
Guardianship Tribunal (NSW) 02 9555 8500
continued >
INTERNET RESOURCES
Below is a selection of useful and interesting websites on both HIV/AIDS and Hepatitis.
This list is not intended to be comprehensive.
HIV/AIDS:
Australian
www.ashm.org.au Australasian Society for HIV Medicine (ASHM):
The peak representative professional body for medical practitioners and other health care workers who work in HIV
and related disease areas. The site contains education, training and conference information as well as ASHM
publications and clinical updates.
www.ancahrd.org Australian National Council on AIDS, Hepatitis C and Related Diseases (ANCAHRD):
Site lists details of committees of ANCAHRD, including Clinical Trials and Research Advisory Committee (CTARC)
and links to CTARC news.
http://www.latrobe.edu.au/www/arcshs/ Australian Research Centre in Sex, Health & Society:
ARCSHS is a collaborating centre to the National Centre in HIV Social Research and is afliated with the
University of Melbourne. It aims to undertake multidisciplinary research into social and behavioural aspects
of sexually transmissible diseases, their prevention and consequences.
www.burnet.edu.au Macfarlane Burnet Institute for Medical Research and Public Health:
Australias largest virology and communicable disease research institute, the Burnet Institute
investigates some of todays most serious viral infections such as HIV/AIDS, hepatitis and measles.
www.med.unsw.edu.au/nchecr/ National Centre in HIV Epidemiology and Clinical Research:
NCHECR is one of Australia's leading medical research centres and is recognised internationally as
a leader in the eld of research into HIV/AIDS and viral hepatitis.
www.arts.unsw.edu.au/nchsr National Centre in HIV Social Research:
NCHSR conducts research which describes and analyses the social understandings, meanings and practices
of peoples, institutions and communities in relation to HIV, STDs and other communicable diseases.
www.hiv.edu.au/ National Centre for HIV Virology Research:
The National Centre for HIV Virology Research is in the process of being re-organised into the new Australian Centre for
HIV and Hepatitis Virology Reasearch (ACH2), which is to be a broadly inclusive, collaborative national virology
research organisation focused on HIV and Hepatitis C.
www.med.unsw.edu.au/ndarc/ National Drug and Alcohol Research Centre:
NDARC is a clearinghouse for a wide range of drug-related research and publications.
International
http://www.aegis.com/ AEGiS (AIDS Education Global Information System):
The largest HIV/AIDS website in the world. AEGiS is a non-prot, charitable and educational corporation with
information for the medically educated and layperson alike, with an easily used search engine and useful online forum.
http://www.aidsmap.com/ AIDSmap:
This site is produced by the National AIDS Manual (NAM Publications) in collaboration with the British HIV
Association and provides extensive information on treatments and a searchable database. Includes The Wheel
an interactive pill planner for consumers and health professionals.
www.aids/org AIDS.ORG:
This US site offers quality HIV/AIDS treatment information and resources .
www.thebody.com/index.shtml The Body: an AIDS and HIV Information Resource:
The Body aims to use the Web to: lower barriers between patients and clinicians; demystify HIV/AIDS
and its treatment; foster community, and improve patients quality of life.
http://www.hivdent.org HIVdent:
Comprehensive coverage of HIV issues and dentistry; also hepatitis C information.
http://hivinsite.ucsf.edu/InSite HIVInSite:
Treatment, prevention and policy information from the University of San Francisco California.
www.hopkins-aids.edu The Johns Hopkins AIDS Service:
This website is provided by the Johns Hopkins University as a resource for physicians and other
health care professionals in providing care and treatment to patients with HIV/AIDS.
www.hiv-druginteractions.org Liverpool HIV Pharmacology Group (LHPG):
This website has been designed for use both by clinicians and patients as a straightforward,
up-to-date reference on anti-HIV drugs.
www.medscape.com Medscape HIV/AIDS:
Medscape is the leading interactive, multi-speciality commercial Web service for clinicians and consumers.
Includes free access to the MEDLINE, AIDSLINE and TOXLINE databases and the HIV/AIDS Clinical Calculator
of drug-drug interactions. http://hiv.medscape.com/Medscape/HIV/DrugInteractions/index.cfm
www.nzaf.org.nz New Zealand AIDS Foundation.
www.unaids.org UNAIDS: The Joint United Nations Program on HIV/AIDS:
As the main advocate for global action on HIV/AIDS, UNAIDS leads, strengthens and supports an
expanded response aimed at preventing the transmission of HIV, providing care and support, reducing
the vulnerability of individuals and communities to HIV/AIDS, and alleviating the impact of the epidemic.
14 Contact and referral information
INTERNET RESOURCES
HEPATITIS :
Australian
http://www.health.gov.au/pubhlth/strateg/hiv_hepc/hepc/index.htm part of the Australian
Government Department of Health and Ageing site, outlining the national response to HCV and providing
links to epidemiological and statistical information, as well as the Australian hepatitis C research register
(http://www.health.gov.au/pubhlth/strateg/hiv_hepc/hepc/register/index.htm)
www.hepatitisaustralia.com Australian Hepatitis Council:
An information resource primarily for people with hepatitis C, their families, friends and carers.
www.acthepc.org ACT Hepatitis C Council
www.hepatitisc.asn.au Hepatitis C Council of Queensland
www.ntahc.org.au Northern Territory AIDS & Hepatitis Council
www.hepccouncilsa.asn.au Hepatitis C Council of South Australia
www.taschard.org.au Tasmanian Council of AIDS, Hepatitis and Related Diseases (TasCAHRD)
www.hepcvic.org.au Hepatitis C Council of Victoria
www.hepatitiswa.com.au Hepatitis C Council of Western Australia
The following organisations can provide information and assistance about hepatitis C and related issues
www.aivl.org.au Australian Injecting and Illicit Drug Users League (AIVL)
www.adf.org.au Australian Drug Foundation
www.multiculturalhivhepc.net Multicultural HIV/AIDS and Hepatitis C Service
International
www.hepfoundation.org.nz Hepatitis Foundation of New Zealand
www.h-r-n.org Hepatitis Resources Network provides physicians with high-quality, balanced
educational resources and access to clinical trials with the goal of improving the quality of life for
people living with chronic viral hepatitis C.
www.who.int World Health Organization.
Patient information - Natural history and transmission of HIV
What is HIV? HIV (Human Immunodeciency Virus) is the virus that causes AIDS.
What is AIDS? Acquired Immune Deciency Syndrome (AIDS).
How does HIV affect people? When a person rst contracts HIV, a u-like illness may occur. In most cases, without
treatment, HIV slowly causes damage to the immune system. The body becomes less
able to ght infection and illness.
As HIV disease advances, a person may develop AIDS. An AIDS diagnosis generally
means that the immune system is severely weakened and that life-threatening illnesses
may occur. These illnesses include infections (e.g. pneumonia) and cancers.
Recently, more effective treatments have become available. However, it is unknown
whether these treatments can indenitely delay the decline of the immune system. Before
these treatments became available it took an average of 812 years after initial HIV
infection for AIDS to develop.
How is HIV monitored? Regular check-ups and blood tests are conducted to monitor the progress of the disease.
viral load indicates viral activity;
CD4 cell count indicates extent of damage to the immune system.
How many people have HIV? In Australia, approximately 20,000 people have been diagnosed with HIV. Over 6,200
people in Australia have died of AIDS.
How is HIV transmitted? HIV is present in certain bodily uids of infected people (i.e. blood, semen, vaginal uids
and breast milk). It may be passed on by sexual contact, any activity that allows a bodily
uid to enter the blood stream via a break in the skin, or from mother to child. It is not
passed on through normal household contact or by kissing.
How is HIV transmission prevented? HIV transmission is signicantly reduced by:
safe sex, which is any sexual activity that does not allow the transfer of one persons
body uids (blood, semen, vaginal uid) into another. This means using condoms and
water-based lubricants for any vaginal or anal intercourse and avoiding oral sex if
there are cuts or sores on the genitals or in the mouth. If sex toys are to shared, they
should be covered by a condom (Chaper 3);
safe injecting using only sterile equipment (needles, syringes, swabs, spoons, llers,
tourniquets and water) to inject each time or thoroughly cleaning equipment where this
is not possible. Alternatively, drugs can be smoked, snorted or swallowed (Chapter 3
and Appendix 4);
interventions during pregnancy and labour, and avoidance of breast-feeding;
standard precautions (Chapter 12).
Appendix 1
Appendix 2
Patient information Natural history and transmission of HBV
What is HBV? HBV is a virus that can cause hepatitis. Hepatitis means inammation of the liver.
What does the liver do? The liver is one of the largest organs in the body and plays an important role in many vital
functions of the body. Some of the livers many functions include:
acting as a lter to remove alcohol and other toxic substances from the body;
processing and clearing drugs and medications;
manufacturing the many chemical substances needed by the body.
How does HBV affect people? When someone is infected by HBV, his/her body produces tiny proteins called antibodies
in an attempt to eliminate the virus. During the rst 45 to 180 days (six weeks to six
months), the person may feel slightly ill or off-colour and develop joint pains. Sometimes
people with HBV develop typical symptoms of hepatitis (fatigue, yellowed skin or eyes).
A very small number of people die within the rst few weeks or months of hepatitis B
infection. Most adults completely recover from hepatitis B infections, while most infected
babies (children under one year of age) will develop chronic HBV infection. The
appearance of particular antibodies is thought to indicate that HBV is eliminated from the
body. Around 24% of infected adults develop chronic infection. A person with chronic
hepatitis B infection is often called a hepatitis B carrier and may be infected for several
decades.
Chronic hepatitis B infection causes no symptoms in many people, but some will develop
long-term liver inammation, liver scarring and liver cancer. This can take decades to develop.
The symptoms are mild for many people. However, for a minority of people, hepatitis B may
be quite debilitating.
How many people have HBV? Approximately 1 out of every 100 Australians carries the hepatitis B virus. This rate is higher
amongst men who have sex with men, injecting drug users and people of certain nationalities.
Around 12% of people from Mediterranean countries, parts of Eastern Europe, and the
former USSR have chronic HBV infection, while this gure is as high as 10% in some
Australian Aboriginal, central African, and South East and East Asian populations. First
generation immigrants usually have similar rates to those of their country of origin.
How do people know what is A liver function test monitors the level of liver enzymes in the blood. If there is damage
happening to their liver? to liver cells, these levels may be raised. Liver function tests are often a poor indicator of
illness outcome. People who want a more detailed and reliable indication of liver damage
should consider a liver biopsy. This is a procedure where a small amount of liver tissue is
taken using a needle.
How is HBV transmitted? HBV is spread through sexual contact or through infected blood or sexual secretions
(semen, vaginal uids) entering someone elses bloodstream. Transmission can occur via
skin piercing (e.g. injecting drug use or tattooing) or the sharing of toothbrushes and
razorblades. If saliva that contains HBV pierces the skin or mucous membrane (e.g. by
biting), transmission may occur. Mother-to-child transmission commonly occurs if
vaccination and immunoglobulin are not administered.
How is HBV transmission prevented? HBV is prevented through vaccination. HBV immunoglobulin is required for newborn
infants of infected mothers and those acutely exposed to HBV.
In addition, HBV transmission is prevented by:
safe sex (Chapter 3);
safe injecting (Chapter 3 and Appendix 4);
continued >
Appendix 3
Patient information Natural history and transmission of HCV
What is HCV? HCV is a virus that can cause hepatitis. Hepatitis means inammation of the liver.
What does the liver do? See Appendix 2.
How does HCV affect people? When someone is infected by HCV, his/her body produces tiny proteins called antibodies
in an attempt to eliminate the virus. During the rst 28 weeks, the person may feel
slightly ill or off-colour. Typical hepatitis symptoms (fatigue, yellowed skin or eyes) are
uncommon with initial HCV infection.
In approximately 75% of initial hepatitis C infections, antibodies do not eliminate the
hepatitis C virus. When the virus is not eliminated, HCV infection is ongoing. This is
called chronic hepatitis C. Most people eventually develop some signs of hepatitis C
illness usually after ten years or so. The symptoms are mild for many people. However,
for a minority of people, hepatitis C may be quite debilitating.
The exact nature and timing of short-term and long-term consequences of HCV
infection are not clear. The most commonly reported signs of hepatitis C illness are
fatigue and/or pain in the upper right side of the abdomen. Only one person in ve
develops severe scarring of the liver or cirrhosis. If it occurs, cirrhosis usually takes
2040 years to develop. Less than one in ten people develop liver failure or liver cancer.
These conditions usually take 2530 years to develop. In a small proportion of people,
the virus can cause problems in parts of the body other than the liver, such as the joints,
the skin and the kidneys.
How many people have HCV? Approximately 12 in every 100 Australians is HCV antibody positive. In Australia, about
80% of people acquire HCV by injecting drugs. Others have acquired HCV from blood
transfusion prior to 1990. HCV is more common in some ethnic groups.
How do people know what is See Appendix 2.
happening to their liver?
How is HCV transmitted? HCV is spread through infected blood entering someone elses bloodstream (e.g. by
sharing injecting equipment, non-sterile tattooing or piercing, and non-sterile medical
procedures). Mother-to-child transmission occurs in less than 5% of cases. Sexual
transmission of HCV is regarded as very rare, although anal penetration or the presence
of blood may increase the risk of sexual transmission.
How is HCV transmission prevented? HCV transmission is prevented by:
safe injecting (Chapter 3 and Appendix 4);
Appendices 13 written by Paul Andrews et al, authors of Chapter 8.
Appendix 4
Safe injecting and cleaning injecting equipment
The sharing of injecting equipment is the single greatest risk factor for contracting HCV among those who inject drugs. There are options
other than injecting drugs, such as smoking, snorting or swallowing drugs, which will signicantly reduce the risk of contracting HCV, HIV
and other blood-borne viruses. If snorting is the alternative mode of administration, the sharing of straws is not recommended due to a
low risk of HCV transmission.
Injecting with sterile For people who do choose to inject drugs, transmission can be prevented through the exclusive
equipment use of sterile ts (needle and syringe), water and swabs (one to swab the spoon and one to swab the
arm), clean lters, a clean/ detachable tourniquet, and clean hands.The injecting space should also be
clean and all blood contact avoided. Sterile equipment is equipment that has undergone a process that
destroys viruses, bacteria and germs. Sterile injecting equipment includes pre-packaged ts, water and
swabs, that are marked as sterile. All other equipment needs to be cleaned with soap and water or with a
swab. Table 3.5 describes safe injecting procedures in detail.
There is no way of eliminating the risk of viral transmission from used syringes. If patients seek advice
about re-using injecting equipment, the need for sterile equipment must be reiterated.
Using cleaned injecting People who decide to inject with a used t must be advised that they risk becoming infected with HIV,
equipment HBV and HCV. In addition, they should be advised that:
using your own t will be safer than a t used by another person;
the more thoroughly a t is cleaned, the less risk of infection;
cleaning is important for people who are already infected with a blood-borne virus
because they can be re-infected with another strain of HCV, HBV or HIV. Re-infection with another strain
of HCV or another hepatitis virus may place added strain on the liver.
How to clean injecting The following are directions on how to clean used injecting equipment. A clean workspace
equipment and a safe area for uid disposal (sink, bin, drain etc) are required. Wash your hands before you begin.
1. Equipment Three separate containers lled with:
a. Clean water from the cold tap, for rinsing the blood out of your t.
Use water from the cold tap - preferably soapy water. This is best for rinsing out blood because water
that is too hot or too cold can cause the blood to congeal and stick inside the t, where it can shed
microscopic particles into your mix.
b. Full strength bleach for soaking/bleaching your t (5.25% sodium hypochlorite).
c. Clean water from the cold tap to rinse the bleach from your t.
2. Cleaning process a. Rinsing:
Rinse the t in clean water from the cold tap from the rst container.
Squirt the water out into your sink or safe uid disposal area.
Repeat until you cannot see any traces of blood.
b. Bleaching:
Use full strength bleach (at least 5.25% sodium hypochlorite and check the use-by date).
Take the t apart.
Soak it completely, covering it with bleach for at least two minutes.
If you can't soak:
Draw the bleach into the t and shake it for at least thirty seconds (or while you count slowly to 30).
Squirt the bleach out into your sink or safe disposal area.
Repeat the process at least once, again counting slowly to thirty (as above).
c. Flushing:
Draw up fresh water from the third container.
Do NOT use water from the FIRST container as this has been contaminated with blood.
Squirt, ushing the water into the safe uid disposal area or sink.
Repeat ushing process until all the bleach has been removed.
FLUSH AT LEAST SIX TIMES.
continued >
3. When you have cleaned
your t follow the
Guidelines for safer
injecting (Chapter 3)
4. Some handy hints for Stock up on equipment so you won't be caught short.
being blood aware Make sure the surface where you prepare your hit is clean.
Wash your hands with warm soapy water before and after injecting. This will remove any traces of
blood from your ngers, as well as any unhygienic dirt.
No matter how well-cleaned, never let your used equipment, or anyone else's used equipment, come
into contact with a group mix. Unless sterile ts are used to mix and divide up, then each member of
the group must have their own water, spoon and lter (as well as their own t).
If someone is going to help you inject, make sure they wash their hands before and after.
It is best to have your own tourniquet that you dont share. Try not to get blood on your tourniquet.
Detachable (medical) tourniquets will make this easier.
Rinse your t in clean water from the cold tap immediately after your hit, even if you are disposing of
it. This will remove most of the blood that is present, and therefore reduce the chance of a virus
staying alive in your t. It will also prevent it from blocking, and help reduce the likelihood of dirty hits
if you have to use the t again.
If you are going to save your t for personal re-use, keep track of it (mark it), and keep it safe.
Wash or swab your spoon after each hit, and wash your tourniquet with soapy water as soon as
possible to remove blood spills.
Always dispose of ts safely, in an approved disposal bin, sharps container or childproof, puncture-
proof container. Whenever possible, return sharps containers/used ts to your local needle and
syringe program.
Do not reuse swabs, lters or opened sterile water: they become contaminated with bacteria and
fungi when exposed to air. Dispose of them in the recommended sharps container you have used to
dispose of your used ts, or place inside two plastic bags (double bagging). Return your sharps
container to your local needle and syringe program. If it is not possible to return your used ts to a
needle and syringe program, you can place the sealed container into the rubbish bin.
Also dispose of blood-contaminated materials as above. If you get blood on your clothes, etc. throw
them straight into the wash with a good measure of washing powder.
Appendix 4 adapted from the Australian Intravenous Leagues Guide to Cleaning Fits, 1999, Australian Intravenous League, Canberra.
Glossary of terms
Ab antibody
ACRRM Australian College of Rural and Remote Medicine
AFAO Australian Federation of AIDS Organisations
Ag antigen
AHC Australian Hepatitis Council
AIDS Acquired Immune Deciency Syndrome
AIVL Australian Intravenous League
ALA Australian Liver Association
ALT alanine aminotransferase or alanine transaminase
ANA antinuclear antibody
ANCAHRD Australian National Council on AIDS, Hepatitis C and Related Diseases
Anti-HAV IgM antibody to HAV Igm signies recent exposure to HAV
Anti-HBc IgM antibody to hepatitis B core antigen signies recent exposure to HBV
Anti-HBe antibody to hepatitis Be
Anti-HBs antibody to hepatitis B surface antigen associated with non-replicative phase
Anti-HCV antibody for HCV indicating infection with HCV has occurred
Anti-HDV IgG and IgM antibody to the hepatitis D virus
APTT activated partial thromboplastin time
ARV antiretroviral therapy
ASHM Australasian Society for HIV Medicine
AST aspartate aminotransferase
BD twice daily
B-cell a type of immune cell
BBV blood-borne virus
BCG Bacille Calmette-Guerin (tuberculosis vaccine)
b-DNA branched deoxyribonucleic acid
CAH chronic active hepatitis
CCR5 chemokine co-receptor on the surface of cells which may be used in HIV-cell fusion
CD4 cell a helper T-cell which carries the CD4 surface antigen. CD4 cells are the primary target of HIV and
CD4 cell numbers decline during HIV disease.
CD8 cell a killer or cytotoxic T-cell which carries the CD8 surface antigen
CMV cytomegalovirus
CNC clinical nurse consultant
DHAC Commonwealth Department of Health and Aged Care
DNA deoxyribonucleic acid
EBV Epstein Barr virus
EIA enzyme immunoassay
ELISA enzyme linked immunosorbent assay
FBC full blood count
GESA Gastroenterological Society of Australia
GGT gamma glutamyltransferase
GI gastrointestinal
GP general practitioner
gp120 glycoprotein on the surface of HIV which binds to the CD4 receptor
gp41 glycoprotein on the surface of HIV involved in fusion between HIV and the CD4 cell
HAART highly active antiretroviral therapy
HAV hepatitis A virus
HBcAb see anti-HBc
HBcAg hepatitis B core antigen
HBeAb see anti-HBe
HBeAg HBV e antigen, a marker of viral replication and infectivity
HBIG hepatitis B immunoglobulin
HBsAg hepatitis B surface antigen, a marker of current infection which persists in individuals who become
carriers
HBsAb see anti-HBs
HBV hepatitis B virus
HCC hepatocellular carcinoma
HCV hepatitis C virus
HDV hepatitis D virus
HIV human immunodeciency virus
HPV human papilloma virus
HSV herpes simplex virus
IDU injecting drug user
IFN interferon
Ig immunoglobulin
INR international normalised ratio (a test of blood clotting)
IV intravenous
IU international unit (measurement)
KS Kaposis sarcoma
LFT liver function test
LKM liver kidney microsomal
MAC Mycobacterium avium complex
MAI Mycobacterium avium intracellulare
ml millilitre
mmol millimole
NCHECR National Centre in HIV Epidemiology and Clinical Research
NHMRC National Health and Medical Research Council
NNRTI non-nucleoside reverse transcriptase inhibitor
NAPWA National Association of People Living with AIDS
NRTI nucleoside analogue reverse transcriptase inhibitor
OI opportunistic infection
p24 a core HIV protein, the primary protein detected by the superceded HIV antigen test
PBS Pharmaceutical Benets Scheme
PCP Pneumocystis carinii pneumonia
PCR polymerase chain reaction
PCT porphyria cutanea tarda
PEP post-exposure prophylaxis
pg/ml picogram per millilitre
PI protease inhibitor
PML progressive multifocal leucoencephalopathy
Qd once daily
RACGP Royal Australian College of General Practitioners
RACP Royal Australian College of Physicians
RF rheumatoid factor
RNA ribonucleic acid
RT reverse transcriptase
SBP spontaneous bacterial peritonitis
Section 100 a section of the Pharmaceutical Benets Scheme which provides access to highly specialised drugs
SMA smooth muscle antibody
SR sustained virological response (negative HCV RNA and normal ALT six months after completion of
therapy for HCV)
SSRI selective serotonin re-uptake inhibitors
STI sexually transmissible infection
T-cell white blood cell or lymphocyte
Td three times daily
l microlitre
U & E urea and electrolytes
VZV varicella zoster virus
WHO World Health Organization
Index
Note: Italic type indicates
information is part of a table or
illustration.
Aborigines, 21, 22, 42, 68
acute HIV infection, 33
acute liver failure, 40, 42, 45
acute necrotizing ulcerative gingivitis
(ANUG), 49
acute retroviral syndrome, 31
acute viral hepatitis, 37-45
adherence to therapy, 15, 53, 71
adolescents, 21, 25, 59
Africa, 11, 22, 47
AIDS indicator diseases, 47, 82
AIDS-related lymphoma, 51, 52
alcohol, 26, 29, 37-39, 50, 56, 57,
58, 61, 72, 73, 84, 85, 85, 89, 89,
91, 93, 97
anogenital warts, 48
anorexia, 37, 55, 57
antiretroviral therapy (for HIV)
commencing, 72, 78, 79
drug chart, 80
early treatment with, 33
interactions, 12, 50, 52, 71,
73, 81
pregnancy, 69
primary infection, 30, 31, 47
side-effects, 12, 35, 46, 50, 51,
69, 79, 80
antiviral therapy (for viral hepatitis),
56, 90, 93
drug chart, 91
side-effects, 93
ANUG (acute necrotizing ulcerative
gingivitis), 49, 50
anxiety, 25, 35, 39, 43, 53, 67, 68,
69, 71, 90
aphthous mouth ulcers, 49
arthritis, 37
arthropathy, 58, 58
ascites, 18, 55, 57, 58, 61, 87, 91,
94, 100
aseptic meningitis, 48
Asia, 11, 13, 22, 45, 49
autoimmune hepatitis, 37, 68, 85, 92
Bartonella, 51
body composition changes, 52
breast-feeding, 22, 44, 69, 88, 119,
120, 121
Campylobacter, 51
cannabis, 98
candidiasis, oropharyngeal, 47, 48,
49, 74
CD4 cells, 30, 46, 47, 75, 78
decline of, 9, 10, 12, 50, 51, 52,
72, 73, 74, 74, 81
surrogate markers, 72, 74
CD8 cells, 30
cerebellar ataxia, 58, 61
cervical cancer, 47, 48
cholestasis, 40
cirrhosis, 9, 10, 12, 13, 14, 18, 37,
54, 55, 56, 57, 58, 61, 73, 84-90,
93, 96, 121
clinical latency, 47
CMV (cytomegalovirus), 47, 50, 51,
51, 72
CMV retinitis, 50, 81
coagulopathy, 58
complementary therapies, 38, 90
compliance, 81, 93
contact and referral information,
113-118
contact tracing, 33, 42
corticosteroids, 40, 90
counselling, 63-70
cross-cultural issues, 29, 68
cryoglobulinaemia, 37, 58
cryptococcosis, 47, 49, 51, 52,
73, 99
cryptosporidiosis, 12, 47, 51, 74
Cryptosporidium, 51
cytokines, 30
cytomegalovirus (CMV), 47, 50,
51, 72
dementia, HIV-related, 47, 52, 74
depression, 65, 82
dermatoses, 48, 49
dermatitis, seborrhoeic, 49, 74
dermatophyte infections, 49
diarrhoea, 17, 47, 51, 72, 79, 82, 100
drug history checklist, 26
drug interactions, 79
drug use, equipment and language,
26
drug use, history, 26
drug use, injecting, 9, 11, 18, 19, 20,
21, 22, 23, 25, 26, 63, 97, 122
drug use, useful questions, 26
Dupuytrens contracture, 61
EBV, 49, 52
encephalopathy, 39, 57, 61, 100
endemic countries, 45
eosinophilic pustular folliculitis, 49
epidemiology, 17-23, 37
equivocal test results, 67, 68
euthanasia, 98
exposure and acute HIV infection,
30-36
febrile syndromes in HIV-infected
individuals, 51
fever, 12, 17, 31, 47, 51, 51, 52, 82
fatigue, 17, 72, 90, 82, 100
brosis, 55, 58, 84, 86, 87
gastrointestinal symptoms of HIV, 31
gingivitis, 49, 50
glomerulonephritis, 37, 58, 58
glossary, 124
gonorrhoea, 16, 19
granulocytopenia, 58
gynaecomastia, 57, 58, 61
haemophilia, 11, 21, 21, 35, 97
harm reduction, 28, 29, 67, 122, 123
HAV, see hepatitis A
HBV, see hepatitis B
HCC, see hepatocellular carcinoma
HCV, see hepatitis C
health care workers, testing and
vaccination of, 104-105
hepatic encephalopathy, 55, 57, 61
hepatitis A (HAV), 37, 38, 39, 40, 45,
42, 43, 90
hepatitis A vaccination, 42, 44, 45,
67, 68, 73, 104
hepatitis, acute, 37-45
hepatitis, autoimmune, 37
hepatitis B (HBV)
assessment of, 17-19
chronic, 37, 54-62
diagnosis, 38, 40, 41
epidemiology, 17-23, 37, 40
exposure management, 103, 104
HBV mutants, 13
HIV coinfection, 50
incubation period, 38
monitoring, 40, 88
natural history, 12, 13, 120
outcomes of acute HBV, 38
perinatal transmission, 11, 12,
20, 21, 22, 23, 44, 69, 120
post-exposure management, 42
post-exposure prophylaxis (PEP),
43, 106
prevalence and transmission, 20,
21-22
prevention, 16, 17, 23, 24, 28,
29, 32, 35, 37, 41, 42, 44, 45, 65,
103, 120
primary infection, 37-45
progression, 55
risk assessment, 18, 19, 20, 64
risk factors for transmission,
19, 22
symptoms and signs of acute
viral hepatitis, 37, 120
testing, 38, 39, 59, 60, 61, 62, 63,
84, 86-88, 104
therapy, 15, 39, 40
transmission, 9, 11, 17-23, 103,
120
treatment, 63, 84, 87-89, 91,
93, 94
vaccination, 23, 44, 44, 45, 63,
65, 67, 68, 73, 90, 104
virology, 10
hepatitis C (HCV), 9, 10, 37-45
acute, 37-45
assessment of, 15, 17-19, 86
chronic, 37, 54-62
coinfection with HIV and/or HVB,
56, 73, 92
diagnosis, 38, 40, 41
epidemiology, 17-23, 37, 40
exposure management, 103, 104
genotype, 9, 59, 84, 87, 91, 92
HIV coinfection, 50, 56
incubation period, 38
injecting drug use, 9, 11, 18, 19,
20, 21, 22, 23, 25, 26, 63, 122, 123
monitoring, 40, 41, 50, 84, 85,
86
natural history, 13, 14, 37-45,
55-61, 120
outcomes of acute HCV, 38
20, 21, 22, 23, 44, 69, 88,121
post-exposure management, 42
43, 106
prevalence and transmission,
19, 20, 21
prevention, 16, 23, 28, 29, 35, 41,
42, 44, 45, 65, 84, 90, 103, 121
prognosis and progression, 14
progression, 55
risk factors for transmission,
19, 22
signs of deteriorating liver
function, 87
symptoms and signs of acute
viral hepatitis, 37, 121
symptoms and signs of chronic
viral hepatitis, 54-62, 121
testing, 17, 38, 39, 59, 60, 61, 62,
63, 84, 86-88, 104
therapy, 15, 39, 40, 90
transmission, 9, 11, 44, 17-23,
103, 121
treatment, 15, 39-44, 85-87,
90-92
virology, 10
hepatitis D, 39, 86
hepatocellular carcinoma (HCC), 9,
10, 12, 37, 54, 55, 58, 87, 90
hepatomegaly, 37, 61
herpes, 17, 19, 47
heterosexual HIV transmission,
21, 23
Histoplasma, 51
history taking, 24-29, 65
HIV
acute infection, 33
acute retroviral syndrome, 31
alarm bells for infection, 48
antiretroviral therapy, 33, 34, 63,
69, 71, 72, 78, 79, 97
assessment of, 17-19, 72, 73, 77
chronic, 46-53, 71
clinical latency, 47, 47
coinfection with viral hepatitis,
73, 92
contact tracing, 33
detecting primary infection, 31
education, 63, 77
epidemiology, 17-23
exposure management, 33,
103-106
global epidemic, 22
heterosexual transmission of,
21, 23
management of, 33, 71
monitoring, 30, 35, 36, 50, 71,
72, 74, 77, 119
natural history, 11, 12, 30, 72,
119
opportunistic infections, 12, 12,
17, 50, 51, 72, 74, 81
pathogenesis of acute infection,
30
pathology tests for diagnosis of
primary infection, 32
20, 21, 22, 23, 69, 119
32, 34, 35, 77, 106
prevalence and transmission, 20,
21
prevention, 16, 17, 23, 24, 28,
29, 32, 35, 63, 65, 66, 69, 73, 76,
103, 119
primary care management of,
71-83
psychological assessment, 65,
69, 70, 76
psychosocial assessment, 66,
70, 75
recent risk exposure, 32
risk factors for transmission, 19,
22
seroconversion illness, 11, 31,
34, 68
supporting newly diagnosed
patients, 33, 34, 66
symptoms and signs of primary
infection, 31, 31, 119
testing, 17, 31, 32, 46, 48, 50, 51,
52, 63-70, 72, 104
therapy, 14, 15, 63
transmission, 9, 11, 17-23, 69,
103, 119
treatment issues, 72, 78
treatment regimens, 63, 79
vaccination, 45, 104
virology, 9
homosexual men, 11, 21, 35, 97
HPV (human papillomavirus), 48
hypogammaglobulinaemia, 48
illegal/recreational drug use, 9, 11,
18, 19, 20-23, 25, 26, 79, 97
immune reconstitution disease, 50
immunisation, 44, 45, 63, 65, 69
immunodeciency, 47, 50, 51, 72
infection control, 102-106
infections, opportunistic, 12, 12, 17,
50, 51, 72, 74, 81, 81, 99
injecting drug use, 9, 11, 18, 19, 20,
21, 22, 23, 25, 26, 63
taking a drug-use history, 26, 63
safe injecting, 27, 122, 123
cleaning injecting equipment,
122, 123
isosporiasis, 47
interferon alpha (alfa), 15, 91, 93
interferon therapy, 15, 40, 50, 59, 91
jaundice, 13, 37, 40, 42, 43, 56, 57,
58, 61, 87
kansasii, 47
Kaposis sarcoma, 47, 47,48, 48, 73
lamivudine, 50, 91, 93, 94
legal issues, 64, 97, 106, 107-112
condentiality, 65, 96, 108
diagnosis malpractice, 111
discrimination, 18, 35, 65, 110
duty of care, 111
negligence, 111
notication, 110
privacy, 109
counselling requirements, 64, 65
leuconychia, 57
lichen planus, 58, 58
lipodystrophy, 15, 79
liver disease, 14, 17, 54, 55-58, 60,
73, 86
liver failure, 9, 14, 18, 37, 38, 40, 42,
45, 54, 55-58, 87, 100
liver function, 50, 54-59, 86, 87
liver transplant, 40, 94
lymphadenopathy, 17, 31, 48
lymphoma, 12, 47, 51, 51, 52, 74
lymphopenia, 47, 48
MAC (Mycobacterium avium
complex), 47, 50, 50, 51, 51, 74,
81, 99
MACS (Multicenter AIDS Cohort
Study), 73
Mediterranean basin, 13
meningitis, aseptic, 48
metabolic disorders, 15, 85
Microsporidium, 51, 74
Molluscum contagiosum, 48, 49
mononeuritis, 58, 58
mouth ulcers, aphthous, 49
Multicenter AIDS Cohort Study
(MACS), 73
Mycobacterium aviumcomplex
(MAC), 47, 50, 50, 51, 51, 73,
81, 99
National Health and Medical
Research Council (NHMRC), 69,
102-105
National Serology Reference
Laboratory, 67
natural history
HBV, 12, 13, 120
HCV, 13, 14, 37-45, 55-61, 120
HIV, 11, 12, 30, 72, 119
needle-stick injury, 20, 103, 104
neurological symptoms, 31, 52, 58,
58, 99
neutropenia, 46, 48
non-Hodgkins lymphoma, 47, 48,
51, 52, 73
non-nucleoside reverse transcriptase
inhibitors (NNRTIs) 78, 80
notication of health authorities,
33, 42, 110
nucleoside analogue reverse
transcriptase inhibitors (NRTIs),
79, 80
nutrition, 89
obesity, 14, 56, 85, 89
opportunistic infections, 12, 12, 17,
50, 51, 72, 74, 81, 81, 99
mild immune deciency, 47
severe immune deciency, 50
oral conditions, 17, 49
oral hairy leukoplakia, 17, 49, 74
oropharyngeal candidiasis, 17, 49
pain management, 98, 99
palliative care, 96-101
palmar erythema, 18, 56, 57, 57, 61
pathogenesis of acute HIV infection,
30
pathology tests for diagnosis of
primary HIV infection, 32
patient information, 119-123
PCP (pneumocystis carini
pneumonia), 31, 47, 50, 51, 73, 99
pegylated interferon, 15, 16, 90, 92
Penicillium marneffei, 49
perinatal transmission, 11, 12, 20,
21, 22, 23, 44, 69, 88
perinatally acquired infection, 22, 54,
69, 120
peripheral neuropathy, 58, 58, 61, 99
peripheral oedema, 58, 87
Pharmaceutical Benets Scheme
(PBS), 35, 40, 59, 71, 86, 91
PML (progressive multifocal
leukoencephalopathy), 47, 52
pneumocystis carini pneumonia
(PCP), 31, 47, 50, 51, 74, 99
pneumococcal
disease, 47, 50, 51
vaccine, 72, 81
pneumonia, 12, 47, 48, 50, 51,
51, 74
polyarteritis nodosa, 58, 58
porphyria cutanea tarda, 58, 58
32, 34, 35, 43
pregnancy, 11, 12, 20, 21, 22, 23, 44,
54, 68, 69, 88, 91, 120
primary HIV infection, 30-36, 47
primary CNS lymphoma (PCNSL), 52
progressive multifocal
leukoencephalopathy (PML),
47, 52
protease inhibitors (PIs), 51, 53, 79,
80, 100
prothrombin time, 38, 59, 61, 86, 87
psoriasis, 48, 49, 74
psychiatric problems, patients with,
29, 65
psychological/psychiatric
assessment, 65, 68, 69, 75, 76, 82
psychosocial issues
acute hepatitis, 43
acute HIV, 33, 36
chronic hepatitis, 90
chronic HIV, 53, 75, 71, 75
palliative care, 96-98
positive diagnosis, 65, 66
public health notication, 33, 42, 110
quasispecies, 10, 11
rashes, HIV-associated, 48, 49
recent risk exposure, 32
referral and contact information,
113-118
retinitis, CMV, 50, 81
retroviral syndrome, acute, 31
ribavirin, 50, 91, 93
risk assessment, 18, 19, 20, 24-29,
64, 65
risk assessment, useful questions
table, 28
risk factors for transmission, 19, 67
safe injecting procedures, 27, 122
safe sex, 28, 29, 34, 35, 119
salmonella, 47, 51
septicaemia, 51
seborrhoea, 49
seborrhoeic dermatitis, 17, 49, 74
seroconversion illness, HIV, 11, 31,
34, 68
serology
HIV-related, 30-33, 46, 47
viral hepatitis, 44, 59, 84, 88, 86
sexual health, 19, 33, 34, 35, 46-53,
76, 77
sexual history, 26-28
shingles, 47, 74
Sjogrens syndrome, 58, 58
skin conditions, 12, 31, 47, 49, 58,
74, 82
SNHL (systemic non-Hodgkins
lymphoma), 52
spider naevi, 17, 56, 57, 57, 61
splenomegaly, 18, 57, 61
squamous dysplasia, 48
standard precautions, 103
steroids, 26, 40, 49, 90
stigma, 35, 63, 71, 75, 96
support services, 35, 36, 62,
113-118
supporting newly diagnosed
patients, 33, 34, 66, 67
symptoms and signs of acute viral
hepatitis, 37
symptoms and signs of chronic HIV,
46-53
symptoms and signs of chronic viral
hepatitis, 54-62
symptoms and signs of primary HIV
infection, 31
syphilis, 72
systemic non-Hodgkins lymphoma
(SNHL), 52
TB (tuberculosis), 12, 47, 48, 51,
72, 81
terminal care, 100-101
testing, 63-70
acute hepatitis, 38, 39
post-test counselling, 63, 66,
67, 68
pre-test counselling, 63, 64, 65,
66
primary HIV infection, 30, 32, 33
therapy, adherence to, 15, 53, 71
thrombocytopenia, 48, 58
thrush, oral, 48, 49
thrush, vaginal, 48
thyroid disorders, 58, 58, 59, 60,
61, 93
toxoplasmosis, 12, 47, 51, 52, 72,
73, 81, 99
transmission of blood-borne viruses,
9, 11, 17-23
tuberculosis (TB), 12, 47, 48, 51,
72, 81
ulcers, mouth, 49
vaccination
health care workers, 104
hepatitis A, 42, 44, 45, 67, 68,
73, 90
hepatitis B, 44, 45, 67, 68, 73, 90
inuenza, 72, 81
pneumoccocal, 72
vaginal thrush, 48
viral load, 46, 47, 50, 56, 59, 72, 73,
74, 75, 76, 78, 79, 103
virology
HBV, 10
HCV, 10
HIV, 9
warts, anogenital, 48
wasting, 100
HIV-related, 47, 72, 82
hepatitis-related, 87, 94
Wilsons disease, 37
women, 19, 20, 35, 69, 75, 76, 91
Other ASHM Monographs
HIV Management in Australasia:
Intended predominantly for registrars, medical students,
specialists, general practitioners and nurses, this respected
monograph is divided into three sections.
The rst deals with basic HIV virology, immunology and the
tools used to monitor HIV disease. The second discusses
antiretroviral therapy. The third section focuses on clinical
presentations, including diagnostic features, treatment,
prevention and outcome.
The 2003 edition was described as: a cornerstone resource
in HIV education for HIV clinicians. The concise, yet
authoritative and clear, style of this publication makes it an
ideal educational tool. (PROFESSOR MICHAEL KIDD)
Published 2004, ISBN 1 920773 10 X
Coinfection
HIV & Viral Hepatitis
a guide for clinical management
This publication reects best practice in Australia today for the
clinical management of coinfection with HIV and viral hepatitis.
The monograph is designed to meet the needs of
medical practitioners working with HIV patients.
It addresses: Hepatitis B coinfection Hepatitis C coinfection
Hepatoxicity associated with antiretroviral therapy.
Copies are available free of charge to specialist care providers,
medical registrars, other health care workers, academics at
medical facilities and other education providers in Australasia.
Published 2003, ISBN 1 920773 05 3
PLEASE USE THIS AS AN ORDER FORM FAX, POST or EMAIL YOUR REQUEST
Title: Given name: Surname:
Occupation: Organisation:
Address:
State: Postcode:
Phone: Fax:
Mobile: Email:
Please post or fax your completed order to ASHM, LMB 5057 Darlinghurst NSW 1300 Australia
Ph: 61-2-8204 0700 Fax: 61-2-9212 2382 Email: ashm@ashm.org.au
Please send me ______ copies of
HIV Management in Australasia
Please send me ______ copies of
Coinfection: HIV & Viral Hepatitis

HIV-Viral Hepatitis - A Guide For Primary Care

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